Archive for the ‘Psychological Aspects’ Category

Antidepressants Cause Severe Withdrawal Symptoms Like “Hallucination,” “Mania,” & Anxiety,” New Study Reveals

Antidepressants Cause Severe Withdrawal Symptoms like “Hallucination,” “Mania,” & “Anxiety,” New Study Reveals

Wednesday, October 3rd 2018 at 6:15 pm

Written By:  Sayer Ji, Founder

© [10/3018] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here”

New research reveals severe withdrawal symptoms in over half of those who discontinue antidepressant drugs, including lasting and even permanent damage.

A concerning new study published in the journal Addictive Behavior and titled, “A systematic review into the incidence, severity and duration of antidepressant withdrawal effects: Are guidelines evidence-based?,” reveals that antidepressants are far more addictive and harmful than previously assumed, and vindicates the long time activism on this issue spearheaded by American psychiatrists like Kelly Brogan, MD and Peter Breggin, MD.

Highlights from the paper are as follows:

  • More than half (56%) of people who attempt to come off antidepressants experience withdrawal effects.
  • Nearly half (46%) of people experiencing withdrawal effects describe them as severe.
  • It is not uncommon for the withdrawal effects to last for several weeks or months.
  • Current UK and USA Guidelines underestimate the severity and duration of antidepressant withdrawal, with significant clinical implications.

This study aimed to assess the veracity of the the U.K.’s current National Institute for Health and Care Excellence and the American Psychiatric Association’s depression guidelines which state that withdrawal reactions from antidepressants are ‘self-limiting’ (i.e. typically resolving between 1 and 2 weeks).

In order to accomplish this goal the systematic review used the following methods:

“A systematic literature review was undertaken to ascertain the incidence, severity and duration of antidepressant withdrawal reactions. We identified 23 relevant studies, with diverse methodologies and sample sizes.”

The results were reported as follows:

“Withdrawal incidence rates from 14 studies ranged from 27% to 86% with a weighted average of 56%. Four large studies of severity produced a weighted average of 46% of those experiencing antidepressant withdrawal effects endorsing the most extreme severity rating on offer. Seven of the ten very diverse studies providing data on duration contradict the UK and USA withdrawal Guidelines in that they found that a significant proportion of people who experience withdrawal do so for more than two weeks, and that it is not uncommon for people to experience withdrawal for several months.”

Side effects were wide-ranging, lasting several months or longer (including permanent dysfunction), such as: 

“Typical AD withdrawal reactions include increased anxiety, flu-like symptoms, insomnia, nausea, imbalance, sensory disturbances, and hyperarousal. Dizziness, electric shock-like sensations, brain zaps, diarrhoea, headaches, muscle spasms and tremors, agitation, hallucinations, confusion, malaise, sweating and irritability are also reported (Warner, Bobo, Warner, Reid, & Rachal, 2006, Healy, 2012). Although the aforementioned symptoms are the most common physical symptoms, there is also evidence that AD withdrawal can induce mania and hypomania, (Goldstein et al., 1999; Naryan & Haddad, 2011) emotional blunting and an inability to cry, (HolguinLew & Bell, 2013) long-term or even permanent sexual dysfunction (Csoka & Shipko, 2006).”

The study concluded:

“We recommend that U.K. and U.S.A. guidelines on antidepressant withdrawal be urgently updated as they are clearly at variance with the evidence on the incidence, severity and duration of antidepressant withdrawal, and are probably leading to the widespread misdiagnosing of withdrawal, the consequent lengthening of antidepressant use, much unnecessary antidepressant prescribing and higher rates of antidepressant prescriptions overall. We also recommend that prescribers fully inform patients about the possibility of withdrawal effects.”

The researchers also noted that the rising numbers of antidepressant prescriptions used throughout the world may be fueled by the antidepressant drug withdrawal side effects themselves:

“As the lengthening duration of AD use has fuelled rising AD prescriptions over the same time period, we must understand the drivers of such lengthening use. The evidence set out suggests that lengthening use may be partly rooted in the underestimation of the incidence, severity and duration of AD withdrawal reactions, leading to many withdrawal reactions being misdiagnosed, for example, as relapse (with drugs being reinstated as a consequence) or as failure to respond to treatment (with either new drugs being tried and/or dosages increased). This issue is pressing as long-term AD use is associated with increased severe side-effects, increased risk of weight gain, the impairment of patients’ autonomy and resilience (increasing their dependence on medical help), worsening outcomes for some patients, greater relapse rates, increased mortality and the development of neurodegenerative diseases, such as dementia.”

The concerning implications of this study to millions around the world who are on antidepressants were immediately recognized by the media, as evidenced by mainstream reporting on the topic with the following headlines:

Thanks to a small but courageous group of professionals who have been raising awareness of the profound, unintended adverse effects of psychiatric drugs and the abject absence of objective criteria for determining “mental disease,” not only are there already resources available to the public today to better understand the dangers of psychiatric drugs, but there are also programs and protocols in place to help those who are on them to come off of them safely and with the support of others who have done the same already. For instance, the program put together by Dr. Kelly Brogan — Vital Mind Reset — has produced powerful outcomes. Take a look at the testimony wall here to learn from the first hand experiences of those who underwent the program and came out drug-free, often with their psychiatric symptoms and comorbid conditions reduced or completely put into remission.

Related reading: 

Sayer Ji is founder of, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.



Approx 4 Min

Excerpt from the documentary “My Kid Is not Crazy.”

PANS/PANDAS Awareness Day was yesterday but I didn’t get the memo until today.  🙂

While disturbing at the beginning, look how antibiotics made all the difference.  Less than four minutes of film that shows how devastating PANS can be.

How many children are slipping through the cracks and are being labeled “mentally ill?”

A prominent Lyme literate doctor in Wisconsin states that approximately 80% of his Autistic, and PANS/PANDAS patients have Lyme/MSIDS.  


Please note the estimate that 1 in 200 children in the USA are affected by it.

You as a family member, friend, or alert medical professional have the ability to share this information when you suspect it.  Speak up.  These kids need our help.

For more:  Despite the fact that published diagnostic guidelines for PANS/PANDAS were created in 2015, but some physicians still feel it’s not legit.

Physicians need to take this disease seriously.

According to Margo Thienemann, MD, clinical professor of psychiatry and behavioral sciences at Stanford, and the lead author of the portion of the guidelines that address psychiatric and behavioral interventions, treatment is at least tri-part:  

  • if infection is present, treat the infection
  • treat close contacts who may be exposing the child to infection
  • treat inflammation, which is thought to cause the brain symptoms





Chronology of Research on Lyme Disease & Dementia, Alzheimer’s, Parkinsons, Autism


Lapenta J1*, Lapenta JM2

1Lapenta, J. Medic Surgeon, Specialty Dermatology, 24 years of exercise. University of Carabobo,   Venezuela. Ceo Dermagic Express 2Lapenta, J.M. Medic Surgeon. University of Carabobo. Diplomat in Facial Aesthetics Occupational Medicine and Prehospital Auxiliary. Resident Doctor Ambulatorio Del Norte Maracay Aragua State. Coo Dermagic Express.

*Corresponding author: Lapenta J, Medic Surgeon, Specialty Dermatology, 24 years of exercise. University of Carabobo, Venezuela, Email:


The Lyme disease or Chronic Erythema Migrans whose first clinical description was made by the scientist Afzelius in the year 1908, and its causative agent the spirochete Borrelia Burgdorferi was discovered 73 years later by Willy Burgorfer in the year 1981, produced by the tick bite of the family Ixodidae, Ixodes scapularis and many others. Among the numerous species described, Borrelia Burgdorferi is disseminated mainly in the United States, Borrelia garinii and Borrelia Afzelii in Europe and Asia as the most involved and described in geographic and population studies. In addition to producing skin lesions in infected people, and multi-organ side effects it is able to reach the human brain and produce dementia, Alzheimer, Parkinson and Autism, events widely discussed today. In this investigation we will make a chronological description of the events that lead to definitely recognize that this spirochete as the spirochete of syphilis, Treponema pallidum which produces neurosyphilis in its tertiary stage, also the Borrelia is able to reach the brain, and produce collateral damage, a term called neuroborreliosis, and among its most lethal effects can cause dementia, Alzheimer, Parkinson and Autism and as a great sequel the so-called post-treatment syndrome of Lyme disease.

Keywords: Lyme disease, Neuroborreliosis, chronic erythema migrans, Borrelia burgdorferi, dementia, Autism, Alzheimer, Parkinson, post Lyme disease syndrome


The main objective of this research is to demonstrate that the Lyme disease produced by the spirochete Borrelia Burgdorferi and its different species, is not just a skin disease. It has been scientifically proven to produce numerous organic manifestations, and in this work we will demonstrate chronologically that this biological agent can conquer the brain, if it is not detected and treated in time produce lethal neurological effects such as dementia, Alzheimer’s, Parkinson, Autism and as a sequel, post Lyme treatment syndrome.


1.) Describe chronologically how it came to the definitive conclusion that the Borrelia Burgdorferi and its pathogenic species in humans can conquer the brain in several of its stages and produce diverse neurological manifestations ranging from meningitis to dementia, Alzheimer’s, Parkinsonism and Autism, including these terms in the so-called Neuroborreliosis.

2.) Describe the neurological clinical manifestations in positive Lyme patients: children of positive Lyme mothers, adults, and adolescents not treated in time, or those who received treatment and showed resistance to it.

3.) The World Health Organization (WHO) in the update of the ICD-11 year 2018 (International Classification of Diseases) included the codes for Lyme borreliosis related to this research: “Lyme neuroborreliosis”, “dementia due to Lyme disease” and “central nervous system demyelization due to Lyme borreliosis”. After our review, we will urge the recognition by this entity of the rest of the proposed codes.


The history of the term DEMENTIA produced by the spirochaete Borrelia Burgdorferi, is longstanding, beginning in the year of 1922 when the French Garin and Bujadoux described a patient with neurological symptoms and meningitis after the bite of a tick; The skin lesion was similar to the Erythema chronicum migrans (ECM), which was first described in 1908 by Afzelius. A similar case was published by Hellerstrom in 1930. [1-3]

Later in 1941 and 1944 Bannwarth described in 26 patients a clinical condition characterized by: lymphocytic meningitis, neuralgia and neuritis that mainly involved facial nerves; only 3 of them associated with stinging by ticks, but years later European researchers found that this syndrome was associated with tick bites and Erythema chronicum migrans (ECM). This condition was described under several names including meningopolineuritis by tick bite (Garin-Bujadoux-Bannwarth), remaining with the definitive name of Lymphocytic meningoradiculitis or Bannwarth Syndrome. [4-6]

To date there are more than 700 [144] articles published on the subject Lyme disease, we will focus on the most relevant, about 200 referring to the issue we are developing, to keep a chronological line in the exact time.



As we said previously, it was in the year 1922 when the French Garin-Bujadoux [1], described a patient with neurological symptoms and meningitis after a tick bite with skin lesion similar to Erythema chronicum migrans (ECM), and then confirmed by Bannwarth in 1941 and 1944 [4], [5], [6] with the description of 26 cases with a symptom characteristic triad: lymphocytic meningitis, neuralgia and neuritis, some associated with tick bites. This clinical picture was later named with the definitive name of meningopolineuritis or lymphocytic meningoradiculitis or Bannwarth syndrome.[1-6]

This fact was 60 years before the discovery of Borrelia Burgdorferi, but the first neurological symptoms related to the Erythema chronicum migrans (ECM) discovered by Afzelius in 1908 [2], [3], had already been described. [3-6]


The first confirmation that Erythema chronicum migrans (ECM) was and is produced by a living agent was discovered and published by Binder and Col. in 1955 who transplanted skin of three patients with ECM to 3 healthy volunteers and these, in the course of 1 to 3 weeks developed the disease. [7] This occurs 11 years after the description of Bannwarth [4], [5] and 33 years after the description of the first case by Garin and Bujadoux. [1]


In 1976 Lefevre JP, and Cols. [8], published 9 cases of meningoradiculitis after tick’s bites and compared them with 56 previously published cases. They found as predominant clinical symptoms:

  • Pain: radiculitis
  • Paralysis: more than 50% of cases: unilateral or bilateral paralysis of the 7th cranial nerve
  • Pyramidal signs
  • Signs of brain irritation: meningitis, neuralgia
  • Cerebrospinal fluid (CSF): pleocytosis.

This means that in these 20 years (1956-1976) about 65 cases of meningoradiculitis associated or not with ticks bite had already been published. [8]


In this year the French Goffinet AM, and Cols. publish a paper on meningoradiculitis produced by ticks, where confirm the previously described symptoms and launch the hypothetical theory that the etiology is a transmission of living agent, as Binder found in 1995 [7], and suggest that it is a virus transmitted by the tick bite. [9]

Still left 3 years for the discovery of the Borrelia Burgdorferi.


This year of 1981 marked a milestone, Wilheim “Willy” Burgdorfer discovered the causal agent of Chronic Erythema Migrans (ECM), a bacterium belonging to the family of spirochetes as Treponema pallidum (syphilis), studying the stomach of a tick of the genus Ixodes daminii collected in the town of Old Lyme Connecticut, United States, which was named Borrelia Burgdorferi in honor of its name. [10], [11]. From the location where the causative agent was discovered (Lyme village) the name of Lyme disease was born. [10], [11].

One year later in 1982. Hindfelt B, and Cols. [12], publish 11 more cases of meningoradiculitis of Bannwarth, of which 50% was associated with tick bites, describing the classic symptoms of this syndrome, (meningitis, neuritis and radiculopathies); and in addition in the cerebrospinal fluid (CSF): mononuclear pleocytosis (lymphocytes), defect of the blood-brain barrier and intrathecal IgG synthesis, expanding the clinical findings of this pathology.

All patients recovered almost completely from their neurological symptoms in 1-2 months, regardless of treatment. [12]


This year was also very important because researchers Skoldenberg B, and Cols. [13], published 21 cases of chronic persistent meningitis of which 4 (19%) had Chronic Erythema Migrans as antecedent and 4 (19%) had been bitten by ticks; neurological symptoms included:

  • Aseptic meningitis
  • Cranial neuropathy (mostly paralysis of the facial nerve)
  • Peripheral motor and sensory radiculopathies
  • Myelitis
  • Cerebrospinal fluid alterations: mononuclear pleocytosis, protein increase, intrathecal IgG synthesis

The symptoms coincide with those previously described for Bannwarth meningoradiculitis [4], [5]. [6], [8], [9], [12], but the authors report a dramatic improvement in all cases when treated with penicillin G for 14 days [13]. This fact confirmed what was stated by previous studies that it was a living agent that caused the disease. [1-13] Spirochetes (Treponema pallidum, syphilis) are sensitive to this antibiotic [17], [18], [19], and Borrelia Burgorferi is a spirochete. [10], [11].


In the year 1984 keep going the publication of cases of meningoradiculitis of Bannwarth associated with Lyme disease, and Pachner AR. and Cols. [14] published a study of 38 cases, emphasizing the neurological aspects from those patients studied between 1976 and 1983. Already began to speak of “Lyme meningitis” with the same characteristics of Bannwarth syndrome (meningitis, neuropathy and radiculoneuritis); in addition to it, among other symptoms already described: headache, stiff neck, and lymphocytic pleocytosis in cerebrospinal fluid (CSF), unilateral or bilateral facial paralysis and weakness of the extremities. [14]

That same year Pfister and Cols. published 4 cases of meningoradiculitis of Bannwarth in Germany, Munich [15], where demonstrate the presence of antibodies against spirochetes of the Ixodes daminii tick in 100% of cases. In three patients, the antibodies were also present in the cerebrospinal fluid (CSF). In one patient, they isolated CSF spirochetes, and demonstrated specific IgG antibodies in serum and CSF against spirochetes. In one case, the spirochete of cerebrospinal fluid (CSF) was isolated morphologically equal to the spirochete of the tick Ixodes daminii; and postulate that Lyme disease and Bannwarth meningoradiculitis have the same etiology: spirochetes. [10], [11], [15].

This study was confirmed by researcher Rayberg B. [16] that same year of 1984 published in Sweden 9 more cases of Bannwarth syndrome where 6 cases (66%) had high titers of antibodies against the Lyme spirochete (Borrelia) and reaffirm the published previously: Bannwarth syndrome and Lyme disease are caused by spirochetes. [10], [11], [15], [16]

This year of 1984 also marks a milestone in the study of Lyme disease and its relationship with spirochetes when the German scientist Weber K. [17], published 4 cases of this disease that presented the reaction of Jarisch-Herxheimer after being treated with antibiotic therapy. This reaction was first described by the Austrian dermatologists Adolf Jarisch and the German Karl Herxheimer in 1895 and 1902 respectively, when they treated cases of syphilis with mercurial. [18], [19]. This reaction only occurs in cases of spirochetosis (syphilis, leptospira and others), and now the newly discovered spirochete Borrelia Burgdorferi [10], [11], [15], [16], [18], [19]

The reaction occurs a few hours after administration of the antibiotic and is produced by endotoxins released by spirochetes at death, and is characterized by: malaise, hypotension, chills, muscle spasms, headache, tachycardia, hyperventilation and exacerbation of lesions in skin. [18], [19]. This reaction was confirmed in later years in the treatment of Lyme spirochetosis. [32], [55], [138], [146], [168]

That same year of 1984, 117 cases were described in New Jersey, studied between 1976 and 1982, of which 86 were adults and 31 children with Lyme disease. Chronic erythema migrans was present in 93% of the cases. The most common late neurological manifestations, in addition to the immediate organic ones (arthritis 26%, and febrile syndrome 45%), were meningitis (10%) and facial paralysis (8%) of the cases. [20]

In the year 1985 the Germans Christen HJ, and Cols. describe 3 cases of meningoradiculitis of Garin-Bujaudox-Bannwarth in children, confirming the previous description, that the Erythema chronicum migrans (ECM) and its neurological manifestations can also affect children. [20], [21]

This same year 1985 the researchers Stiernstedt GT, and Cols. in 41 out of 45 cases of spirochetal meningitis (91%), prove that the enzyme-linked immunosorbent assay (ELISA) was highly sensitive to the diagnosis of spirochetal meningitis. Also the indirect immunofluorescence method in serum and cerebrospinal fluid (CSF) with 98% of positivity. [22]

It was in this decade that the term “Neuroborreliosis” began to be used in relation to the neurological manifestations of Erythema chronicum migrans (ECM) or newly “named” Lyme disease, when the causative agent was discovered; and many of the works had already been described about meningoradiculitis or Bannwarth syndrome associated with tick bites, and its neurological manifestations. But really the term “Neuroborreliosis” was born in the year 1922 (63 years before) when Garin and Bujadoux described the first case [1], later confirmed by Bannwarth in 1941 and 1944. [4], [5].

This fact that the French Garin and Bujadoux were the first to describe Lyme neuroborreliosis has tried to be disqualified by some authors [172], but definitely the majority of the scientific community does recognize them.

Still left a year before the description of the first cases of dementia associated with Lyme disease [23], fact that marked a milestone and revealed that the neurological damage produced by Borrelia Burgdorferi went beyond the meningoradiculitis of Garin-Bujadoux-Bannwarth Classically described. [1], [4], [5]. [6], [8], [9], 12]


Another important year in the timeline of this research on the association of Lyme disease with dementia. The scientist MacDonald A.B. [23], published for the first time two cases where spirochetes were identified in brain tissue subcultures in the autopsy of two patients who died from dementia, using indirect immunofluorescence and monoclonal antibodies specific for Borrelia species, which had previously been identified by ”dark field” light microscopy.

The cases were a 74-year-old woman with mild dementia of less than 1 year’s duration living in Florida and New York, and the other a 69-year-old man who died in a nursing home in Texas after a history of progressive dementia. 4 to 5 years; him also presents symptoms of Parkinson’s. [23]

This fact was confirmed that same year (1986) by Willy Burgdorfer (discoverer of the spirochete) and Reik L. Jr. [24], who published 8 positive Lyme cases with neurological abnormalities where they found high titers against Borrelia species. Neurological symptoms included:

  • Aseptic meningitis
  • Encephalitis
  • Cranial neuritis
  • Motor and sensory radiculitis
  • Myelitis
  • Severe encephalitis that resulted in dementia in two (2) of these patients
  • Irreversible myelopathy in one (1) patient

These last two findings enlarged the neurological spectrum already known by Borrelia Burgdorferi infection; [12-24].

On the other hand no patient showed the classic marker of the disease that is the Chronic erythema migrans (ECM) and only 3 had arthritis, which is the other clinical marker of this pathology. This fact led them to conclude that Lyme disease can present as pure neurological forms, without extra neural characteristics [24].


In 1987, articles on Bannwarth’s meningoradiculitis and its relation to tick bite, enlargement of the neurological spectrum, (chronic encephalomyelitis, late neuroborreliosis, and findings of IgG anti Borrelia antibodies in the cerebrospinal fluid by ELISA) continue to be published; [26-32] but in addition to this, another important fact occurs:

This year in the timeline of Lyme Neuroborreliosis and its relationship with Alzheimer’s disease was demonstrated, because the researcher MacDonald A.B and Col. [25], published a case of a patient who died of Alzheimer’s which I performed an autopsy of the brain tissue and found the spirochetes of Borrelia in the cerebral cortex. The authors propose that, as in tertiary or late syphilis, Borrelia species invade the brain and remain there for years, subsequently causing dementia; state that an undetermined number of patients with Alzheimer’s disease have late tertiary neuroborreliosis. [25].

This fact: Lyme’s relationship with Alzheimer’s was later shown in other studies that we will mention later [79], [81], [87], [107], [128], [135], [165], [170], [186].

Also this year of 1987 Moore JA, reports again the reaction of Jarisch-Herxheimer in the treatment of Lyme Borreliosis. [32]


For this year, the French Dupuis MJ. [33] published a study describing the three stages of Lyme disease and its neurological manifestations, making a summary of the symptoms, mostly already described previously:

Stage 1 during the first month is characterized by Chronic erythema migrans and associated manifestations.

Stage 2 includes neurological symptoms:

  1. Classic meningoradiculitis. (Garin-Bujadoux-Bannwarth syndrome)
  2. Lymphocytic meningitis with acute or recurrent course.
  3. Facial paralysis
  4. Neuritis of other cranial nerves
  5. Cranial polyneuritis
  6. Sign of Argyll-Robertson
  7. Affectation of peripheral nerves
  8. Acute transverse myelitis
  9. Severe encephalitis
  10. Myositis

Stage 3 of the disease: neurological symptoms, months or years after the disease has started:

  1. Chronic neuropathy with mainly sensory or motor signs
  2. Recurrent cerebrovascular accidents
  3. Cerebral angiopathy
  4. Progressive encephalomyelitis
  5. Ataxic and spastic March. (Parkinson’s symptoms)
  6. Dysfunction of the cranial nerve that includes optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy
  7. Simulation of other diseases: multiple sclerosis
  8. Lesions of the multifocal and mainly peri-ventricular white substance
  9. Psychic disorders: acute presenile dementia.

The author states that high doses of the antibiotic penicillin can stop the disease and sometimes induce regression. [33]; also affirms the great similarity between Borrelia burgdorferi and Treponema pallidum (syphilis) [17], [18], [19], considering it as the “great imitator” of other diseases. [33]


This year of 1989 the researcher Pachner AR and Col. [34], contribute in the classification of the neurological spectrum of Lyme disease by publishing an article where they consider that Borrelia Burgdorferi and its species are highly neurotropic and classify neuroborreliosis in two types:

– Lyme meningitis in the second stage of the disease, which resembles aseptic meningitis; it is often associated with facial paralysis, peripheral nerve involvement and / or radiculopathies and may be the first manifestation of the disease even without the presence of Chronic erythema migrans (ECM)

– The third stage: parenchymal disease which causes a multitude of nonspecific manifestations of the central nervous system (CNS) that can be confused with conditions such as multiple sclerosis, brain tumor and psychiatric disorders.

The authors consider that the “new great imitator” of the diseases is “Lyme borreliosis”, a term attributed ancestrally to another spirochete, Treponema pallidum, causal agent of syphilis; confirming what was stated in the previous study [33], [34] and also in relation to the fact that the neurological manifestations of Lyme disease occurs in stages 2 and 3 of the disease fundamentally.

The scientist Kristoferitsch W. and Cols. describe in that year the characteristics of the neuroborreliosis, type meningoradiculitis of Bannwarth in Europe and affirm that the characteristics are very similar to those presented by the American patients (US) [35].

Pizzarello LD, MacDonald and Cols. [36], published a case of loss of vision in a 71-year-old patient due to temporal arteritis, biopsy and blood culture were performed where spirochetes compatible with Borrelia spices were found. After treatment with iv ceftriaxone the patient showed a moderate improvement. The authors considered this case as the first one where Borrelia is found in a biopsy of the temporal artery. [36]

That same year the Germans Bialasiewicz AA, and Cols. [37] published a case of a 25-year-old female patient who presented with a neurorretinitis in the left eye, later confirmed by Borrelia Burgdorferi, presenting affectation of both eyes, finding advanced atrophy of the optic nerve, visual acuity decrease; magnetic resonance shows multiple demyelinating lesions for ventricular and subcortical areas. This case was considered by the authors to be the first in the literature describing demyelinating lesions in the brain with bilateral optic neuritis verified serologically. The patient improved after receiving treatment with doxycycline. [37]

This fact of the demyelination caused by the Borrelia Burgdorferi was confirmed that same year of 1.989 when Meier C, and Cols. [38], publish a work on 8 patients with neurological complications of the peripheral nervous system produced by Lyme Borreliosis. More than 60% of the patients presented the classic meningoradiculitis of Garin-Bujadoux-Bannwarth. In the biopsy of the nerves it was found:

– Macroscopic infiltrations of epineural vasa nervorum and small infiltrations around of endoneurial capillaries: lymphocytes, histiocytes and plasma cells.

– Thrombosis and recanalization in some epineural vessels.

– Seven biopsies showed a significant loss of myelinated axons due to axonal degeneration.

– In one biopsy they observed segmental demyelination with axonal degeneration.

The authors conclude that the peripheral neurological manifestations of Lyme Borreliosis are angiopathic due to vasa nervorum vasculitis and mainly caused by axonal degeneration. [38] This fact, demyelination of the nerves, also in the brain appears for the first time in our timeline [37], [38] and further broadens the clinical spectrum of neuroborreliosis.

Still left nearby 3 decades in our timeline and already by this date (1.989) the term “Neuroborreliosis” of Lyme had been recognized and among the neurological manifestations of our research: dementia [23], [24], [33], Alzheimer [25], Parkinson [23], [33], they were already described; and in addition to this: central and peripheral demyelination of nerve cells [37], [38] associated with Borrelia Burgdorferi.


Many studies were carried out this decade [39-62], since the potential damage that Borrelia can cause in both the central nervous system (CNS) and the peripheral nerves was already known, so the scientists focused their studies in this line; we will mention the most outstanding ones.

The investigator Judith Miklossy in 1990 [39] describes the neuropathological findings of a case with Lyme neuroborreliosis, manifested as chronic meningitis; there were meningovascular and parenchymal occlusive changes similar to those that occur in tertiary syphilis or neurosyphilis; and suggest that the case described represents the meningovascular form of Lyme or tertiary neuroborreliosis, confirming previous studies [25], [33], [34].

In the year 1991 Krupp, L.B, and Cols. [42], describes 15 patients treated for Lyme Borreliosis who complained of persistent cognitive difficulty after 6 to 7 months of treatment with antibiotic therapy; they were compared with 10 healthy controls. Post-Lyme patients showed a marked deterioration in cognitive tests: memory loss mainly in selective recognition; attributed this finding to chronic encephalopathy produced by Borrelia. This study was confirmed in 1995 by Benke T. and Cols. [50], in 1997 by Gaudino EA. and Cols. who also made a differentiation between this syndrome and chronic fatigue syndrome (SCF). [55] In 1999 Elkins LE. and Cols. also confirmed this fact. [61]

Perhaps this represents the first study [42], about what later was and is called post-treatment Lyme disease syndrome (PTLDS), or Post-Lyme syndrome (PLS) because patients were evaluated months after receiving treatment and presented neurological damage symptomatology in this case chronic encephalopathy. [42], [50], [55], [61]

In the year 1993 Fallon B.A. and Cols. [44], published three cases (3) of neuroborreliosis associated with depression, previously described [33], but patients showed panic attacks and mania; considering these last symptoms as the first reported associated with Lyme neuroborreliosis. [44]

In the year 1994 Schaeffer S, and Cols. publish an article on Lyme disease associated with dementia [48], in 1995 Waniek C, and Cols., report another neuropsychiatric case [49] with fatal outcome of progressive frontal lobe dementia, where pathologically severe subcortical degeneration was found, and reaffirm the fact that Lyme disease can present as pure neurological forms. [24], [48]; the patient improved with antibiotic treatment, but then relapsed.

Now we will put a summary of the neurological findings described in this decade related to Lyme Borreliosis, apart from the classic triad of lymphocytic meningoradiculitis or Garin-Bujadoux-Bannwarth syndrome (meningitis, neuritis and radiculopathies), and the detection of spirochete in cerebrospinal fluid (CSF) and its changes, already widely discussed:

1.) Progressive dementia. [48, [49]

2.) Depression: 26-66% of cases. [43] [46], [54], mania. [44], panic attacks. [44], [60]

3.) Memory disorders [43], [50], [54], [58], [59]: verbal memory, mental flexibility, associative, verbal and articulation functions; decreased consciousness, mental confusion.

4.) Encephalitis, encephalomyelitis, isolated transverse myelitis, vasculitic cerebral disorders. [43], [49], [50], [54]

5.) Paranoia, schizophrenia, bipolar disorders, obsessive-compulsive disorders. [46]

6.) Hallucinations, nightmares, hypersexuality. [52]

7.) Sleep disorders, fatigue. [54], [59]

8.) Jarisch-Herxheimer reaction, post-treatment with antibiotics (amoxicillin). [56]

9.) Hemiparesis, hemianopsia, stenosis of cerebral arteries. [58]

10.) Sensitivity to light, touch and sounds. [60]

The highlights in this decade were the appearance of new neurological symptoms associated with Borrelia Burgdorferi infection, which led to it being considered a “neuropsychiatric” disease, the appearance of the Post-treatment syndrome of the disease (PTLDS) or (PLS) ), and the appearance of new laboratory techniques to detect the causative agent [62].


Already for this decade Lyme neuroborreliosis was widely recognized by scientists worldwide. There were numerous studies [63 – 97] of which we will highlight the most important in relation to our research.

In the year 2001 Tager F.A. and Cols. published a study on 20 children with a history of cognitive complaints after having Lyme disease compared with 20 healthy children. The Lyme positive children presented more cognitive and psychiatric disorders than the healthy ones, being the most relevant: anxiety, depression and fatigue. [66]

In the year 2003, Cassarino D.S. And Cols. [72] published a case of a 63-year-old male patient who presented Erythema Migrans rash, which was detected against Borrelia Burgdorferi antibodies in serum and cerebrospinal fluid (CSF). Clinically I present joint pains and tremors. He was diagnosed with clinical Parkinsonism by several neurologists and subsequently had a fatal outcome. In the cerebral autopsy it was found:

– Mild atrophy of the basal ganglia.

– Depigmentation of the substantia nigra.

– Extensive neuronal loss.

– Extensive loss of the neuronal black substance.

– Astrogliosis

– Absence of Lewy bodies.

– Ubiquitin-positive glial cytoplasmic inclusions in striatal and nigral oligodendroglia.

The authors considered this case as the first report of striatonigral degeneration in a patient with Borrelia burgdorferi infection of the central nervous system and clinical Parkinsonism associated with Lyme. [72] Already the symptoms of Parkinson’s had been previously reported [23], [33].

In the year 2005, Jones CR. and Cols. [76] present a study on the clinical manifestations of 102 children born to Lyme-positive mothers, the most notable neurological clinical symptoms being the following:

1.) Fatigue and lack of resistance: 72%

2.) Orthopedic disorders: sensitivity (55%), pain (69%) spasms and generalized muscle pain (69%), rigidity and / or retarded motion (23%).

3.) Neurological disorders:

A- Headaches: 50%

B-) Irritability: 54%.

C-) Bad memory: 39%

4.) Delay in development: 18%

5.) Seizure disorder: 11%

6.) Vertigo: 30%

7.) Tic disorders: 14%

8.) Involuntary athetoid movements: 9%.

9.) Earning disorders and humor changes: 80%

A-) Cognitive speaking: 27%

B-) Speech delay: 21%

C-) Reading-writing problems: 19%

D.) Problems of vocal articulation: 17%.

E-) Auditory / visual processing problems: 13%

F-) Word selection problems: 12%

G-) Dyslexia: 8%

10.) Suicidal thoughts: 7%

11.) Anxiety: 21%

12.) Anger or rage: 23%

13.) Aggression or violence: 13%

14.) Irritability: 54% -80%

15.) Emotional disorders: 13%

16.) Depression: 13%

17.) Hyperactivity: 36%

18.) Photophobia: 40-43%

19.) Ocular problems: posterior cataracts, myopia, stigmatism, conjunctive erythema (Lyme eyes), optical nerve atrophy and / or uveitis: 30%

20.) Sensitivity of skin and noise (hyperacuity): 36-40%

21.) Autism: (9%). [41]

Autism related to Lyme disease appears in the timeline (2.005), which was confirmed by subsequent studies [93], [95], [117], [124], [125], [130], [179]

Bransfield, R.C. and Cols. publish a study in the year 2008 where they state that chronic infections, including Borrelia burgdorferi and others transmitted by ticks, produce a weakened state in children, either in fetal development or during development that may promote an autistic state. Positive reactivity was found in several patients with autism spectrum disorder for Borrelia Burgdorferi in several studies of 22%, 26%, 20% – 30% and 50% for Mycoplasma, [93]; later the same author published in the year 2009 another work confirming this event and names as possible causal agent of this infectious spectrum:

Babesia, Bartonella, Borrelia burgdorferi, Ehrlichia, Human herpesvirus-6, Chlamydia pneumoniae and Mycoplasma (in particular Mycoplasma fermentans). [95]

In the year 2006, MacDonald A.B. [79], publishes a paper in which he hypothesizes that the rounded forms of Borrelia Burgdorferi are the main cause of rounded structures called “plaques” in the brain affected with Alzheimer’s disease (AD); these are emblematic and are observed as rounded amyloid forms of brain damage in Alzheimer’s. [79]

The same author (MacDonald) in the year 2007 publishes another study where he reaffirms his theory that the “neurofibrillary tangles” present in Alzheimer’s disease are produced by a chronic infection, in this case the Borrelia burgdorferi, mentioning a pilot study where it was demonstrated that seven (7) out of ten (10) Alzheimer’s cases showed positive signs for infectious DNA in the neurons analyzed. [81]; remember that this author in 1987 found Borrelia Burgdorferi in the brain of one patient who died of Alzheimer’s disease. [25]

In the year 2008, Judith Miklossy reaffirms what MacDonald presented, publishing a paper that concludes that bacteria, including spirochetes (Borrelia, Treponema) contain amylodogenic proteins; that cortical deposition of beta-amyloid-peptide (Abeta) and tau phosphorylation can be induced after chronic infections, which produce inflammation of the brain, cytokine release, apoptosis, generation of free radicals, release of nitric oxide and activation of complement, which generate a cascade of events that finally produce the amyloidogenesis typical of Alzheimer’s disease. The author proposes that the treatment with antibiotics and anti-inflammatories in these cases is vital to avoid dementia. [87]

In that year of 2008, Judith Miklossy herself published another work on the neuropathology of dementia in syphilis and Lyme disease, where she emphasizes and reaffirms that both Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme), both spirochetes, in later stages cause dementia, cortical atrophy and deposition of amyloid in the brain. These manifestations may occur years or decades after the primary infection and in the tertiary stage is where the dementia develops apart from other neurological symptoms. [88]

Other studies conducted in this decade reported associated with neuroborreliosis: spontaneous hemorrhage of the temporal lobe [64], posterior column dysfunction [65], headache, loss of sleep, mild ataxia, dysfunction of perception, abnormality in the tendon reflexes, disturbances of sensory responses, memory deterioration, alteration of thoughts [67], personality disorders, anxiety and affect changes [91, paranoid and depressive syndrome. [92]

Summary of this decade with Lyme neuroborreliosis: neurological manifestations in children, association with Alzheimer’s, Parkinson’s and Autism. The so-called post-treatment Lyme disease syndrome (PTLDS) also appears in the timeline.


In this last decade, Lyme disease became known worldwide and studies in relation to it and its consequences in the affected population increased markedly. [98-208]

The dementia associated with Lyme neuroborreliosis was confirmed in several studies [105], [128], [160], [193], corresponding to the years: 2011, 2014, 2016 and 2018.

In relation to Autism associated with Lyme disease, studies were published in this decade in 2012, 2013, 2014, 2017, 2018 with evident evidence that infection by the spirochete Borrelia burgdorferi predisposes children of Lyme positive mothers to present the spectrum autistic, because it has been scientifically demonstrated that this spirochete crosses the placenta [203], [207], and can conquer the fetal brain producing neurological damage in the short and long term in pregnant women, who did not receive adequate treatment, and even after receiving treatment with moderate answers; [117], [24], [125], [130], [179] this fact had already been previously described. [76], [93], 95]

Regarding the association of Alzheimer with Neuroborreliosis, highlight the researcher Judith Miklossy, who published 3 studies, years 2011, 2015, 2016, shows convincing evidence that infection by spirochetes such as Treponema pallidum (syphilis) and Borrelia Burgdorferi, (Lyme) chronically infecting the brain, produce the Beta-Amyloid peptide characteristic of this disease. [107], [135], [165]

In 2017 we published a paper in which we demonstrated the effectiveness of the antibiotic Minocycline in Alzheimer’s disease and other neurological disorders, such as Parkinson’s and Multiple Sclerosis, which would confirm the infectious theory as part of the etiology of these diseases [192]; Other neurological disorders where Minocycline proves to be effective are: schizophrenia, bipolar disorders and autoimmune encephalomyelitis [192]. Here the reflection is unique: if an antibiotic improves a neurological condition, it is because you have an infection (bacteria) in your bloodstream and brain.

Lyme disease showed over time that it does not respect creeds, races, sports and professions by infecting movie celebrities, singers, presidents of nations, and athletes; we present them in this decade, because most of them were in recent years that manifested their illness when Lyme disease was already a notorious event in society. Among them are: Thalia (Mexican singer), 2007; Richard Gere (actor) 1999; Alec Baldwin (actor) 2011; Avril Lavigne (Canadian Singer); 2012; George W Bush Jr. (Former President of U.S.) (2007); Jennifer Capriati (tennis player) 2013; Yolanda Hadid (TV Actress) 2012; Ben stiller (Actor) 2010; Kris Kristofferson (Actor and singer) 2006; Ashley Olsen (Actress) 2012, and many more. [155], [156, [157], [158], [169]. These people are human beings; in no previous study they have been mentioned, they were omitted.

Of these cases, the singer and actor Kris Kristofferson deserves special mention. Since the year 2006 he was bitten by a tick and later developed neurological disorders that led him to present loss of memory; He was missdiagnosed with Alzheimer’s disease and received treatment with two medications without improvement. Later he was diagnosed with Lyme and after receiving antibiotic therapy began to “recover” the memory, considered by some as a true “miracle” and “come back”. It was not a “miracle” his bloodstream and brain were infected with Borrelia Burgdorferi. Today recovered, is 82 years old and continues to sing. [170], [171]

In year 2017, the Ad-Hoc Committee for the recognition of the ICD-11 codes (International Classification of Diseases year 2018) of Lyme disease was established by the social activist Luché-Thayer, J. and recognized scientists [177], who in March of that year describe the first spectrum of all the clinical manifestations of the disease. Subsequently, in august of the same year, published “The situation of human rights defenders of patients with Lyme disease and Recurrent fever.” For that moment I joined the crew as an expert reviewer. [208]

This fact led us to publish in January 2018 the full spectrum of Lyme disease under the name of “Understanding Lyme Disease, classification and codes” [190]; which we expanded with a second publication where we included aspects that were missing such as the post-treatment Lyme disease syndrome (PTLDS), [191] described in the 90’s, [42], [50], [55], [61], and subsequently reviewed in numerous studies [101], [109], [119], [126], [136], [159], [162], [180], [183]; and immunological aspects related to the HLA antigens (major histocompatibility complex), which shows the relationship of the HLA-DR-4, HLADR-2, and HLA DRB1 alleles, with greater susceptibility to Lyme disease, Lyme arthritis and resistance to treatment with antibiotic therapy [45], [68], [75], [80], [118], [191].

In august of 2018 Bransfield Robert. C. publishes a compilation of practically the entire neuropsychiatric spectrum of Lyme disease, [203] already described by him in other studies [83], [90], [93], [95], [115], [116] , [117], [125], [130], [132], [144], [163], [164], [176], [185], [203]. He concludes that there are three ways in which Borrelia Burgdorferi infects the brain causing neuropsychiatric symptoms:

1.) The meningovascular form associated with cerebral vascular infarcts.

2.) Infection within the central nervous system (CNS) which is the atrophic form of Lyme meningoencephalitis and is associated with cortical atrophy, gliosis and dementia.

3.) Infection outside the central nervous system (CNS) that causes immunological effects within the central nervous system (CNS) and other effects that contributes to neuropsychiatric symptoms [203], among those who stand out:

Developmental disorders, autism spectrum disorders, schizoaffective disorders, bipolar disorder, depression, anxiety disorders (panic disorder, social anxiety disorder, generalized anxiety disorder, posttraumatic stress disorder, intrusive symptoms), eating disorders, decreased libido, sleep disorders, addiction, opioid addiction, cognitive impairment, dementia, seizure disorders, suicide, violence, anhedonia, depersonalization, dissociative episodes, derealization [203]; most of them described previously.

This year of 2018 the World Health Organization recognized in the ICD-11 (International Classification of Diseases year 2,108) the following codes for Lyme disease: [206]

– IC1G.0: Early Lyme cutaneous borreliosis.

– IC1G.1: Disseminated Lyme borreliosis.

– IC1G.10: Lyme neuroborreliosis.

– IC1G.11: Carditis due to Lyme.

– IC1G.12: Ophthalmic Lyme Borreliosis.

– IC1G.13: Lyme arthritis.

– IG1G.14: Late cutaneous Lyme borreliosis.

– IC1G.1Y: Other specified disseminated Lyme Borreliosis.

– IC1G.1Z: Disseminated Lyme borreliosis unspecified.

– IC1G.2: Congenital Lyme Borreliosis.

– IC1G.Y: Other specified Lyme Borreliosis.

– 6D85.Y: Dementia due to Lyme disease.

– 9C20.1: Infectious panuveitis in Lyme disease.

– 9B66.1: Infectious intermediate uveitis in Lyme disease.

– 8A45.0Y: Central nervous system demyelination due to Lyme borreliosis.


– Lyme “neuroborreliosis” was not born in the 80s when it began to be mentioned in scientific studies after its causative agent, the Borrelia Burgdorferi was discovered by Willy Burgoderfer in 1981 and its presence in the human brain was later confirmed. He was born in 1922 when the French Garin and Bujadoux described for the first time the meningoradiculitis lymphocytic with its neurological manifestations.

– We demonstrate chronologically and scientifically that Borrelia Burgdorferi and its species can conquer the human brain and produce dementia, Parkinson’s, Alzheimer’s and Autism.

– Unlike Treponema pallidum, which only in the tertiary stage of syphilis is when it produces dementia (neurosyphilis); Borrelia Burgdorferi (Lyme) in its secondary and tertiary stage produces neuropsychiatric manifestations (neuroborreliosis).

– Lyme disease can present as pure neurological forms, without the presence of Erythema chronicum migrans (ECM); this fact is what in many cases makes the diagnosis difficult.

– Several highly specific diagnostic tests appeared to detect Borrelia Burgdorferi, even surpassing those proposed by the CDC.

– The World Health Organization (WHO) recognized the code “Lyme Neuroborreliosis”, “Dementia due to Lyme” this year of 2018 in the ICD-11 and the “demyelination of the central nervous system due to Lyme borreliosis”

– Clinical diseases not recognized: “Alzheimer due to Lyme”, “Parkinson due to Lyme”, but assuming that “dementia” is a common symptom of Alzheimer’s, its tacit recognition is understood; like the case of Parkinson’s, because the demyelination of the central nervous system and the chronic infection of the brain by Borrelia species can cause symptoms of Parkinsonism. Also the “Autism due to Lyme” was not recognized but like the previously described, it is supposed to be included in the term “neuroborreliosis due to Lyme”

– The post-treatment Lyme disease syndrome (PTLDS), was not recognized by the WHO; it was extensively reviewed in this research and which was described more than 20 years ago, will be the subject of a forthcoming investigation.

– Finally, the Lyme disease, now it is not only a dermatological disease, is a neuropsychiatric illness that can easy destroy your brain, if it is not detected and treated at time.


If we include Alzheimer’s disease, Parkinson’s disease and Autism within the spectrum “Lyme neuroborreliosis” code, only post-treatment Lyme disease syndrome (PTLDS) will be left out in this investigation.


To the scientists who with their consecration to the investigation since this disease were described, have managed to reach the bottom and clarify many questions about this disease.

To organizations that struggle every day for society to understand how dangerous this disease is, the need for early diagnosis and adequate treatment; and how to prevent the tick bite.

To my son, and father, motors of the  real “machine” Dermagic Express of these investigations, which we dedicate to the entire world population.


**Comment from me**

The chronology of how this has played out is important for two reasons – 1) Research has shown for decades how serious this illness(es) is.  Again, prudence would err on the side of caution and further research on ALL of these areas should have been conducted long ago.  If this were Zika (a big money maker) trust me, research would be conducted with abandon.  2) The paper trail with tangible proof only supports the belief that there are reasons WHY all of this continues to be ignored allowing thousands and thousands to suffer alone.  

My only other comment is that we still don’t know many things and would be amiss in putting it all in a nice box with a bow on it.

For instance, while there are 3 stages of Lyme, people can hop around within these stages in no certain order.  One little girl within 4-6 hours of tick bite couldn’t walk or talk:  It didn’t take her days, weeks, or months to have this cross into the central nervous system.  We need studies showing if tick bite LOCATION has anything to do with this.  She was bitten above her eye.  Since that’s in close proximity to her brain, it would make logical sense for her to potentially have neurological symptoms quickly but no research to date spells this out.  YET WE NEED TO KNOW.

My own personal story is that of gynecological symptoms first which then radiated out everywhere:

Many claim to be infected in untero, yet the authorities deny, deny, deny this, despite much evidence:



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155.) Kelly Lawler, USA TODAY Published 10:04 a.m. ET Nov. 12, 2015 | Updated 10:05 a.m. ET Nov. 12, Avril Lavigne on her Lyme disease: ‘I’m coming out on the other side’  Source:

156.) La Nacion 1 de julio de 2015  • 17:29. Otros famosos que padecieron la rara enfermedad de Avril Lavigne. Source:

157.) Fox News. OUTBREAKS July 31st, 2015‘In the Lyme light’: 10 celebrities diagnosed with the painful tick-borne disease Source:

158.) The Pop Mythologist  April 2, 2015. 19 celebrities who have struggled with Lyme disease Sorce:

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171.) Dana Parish, Contributor. A Slow Slipping Away”— Kris Kristofferson’s Long-Undiagnosed Battle with Lyme Disease. Source:

172.) Gary P. Wormser and Vanessa Wormser. Did Garin and Bujadoux Actually Report a Case of Lyme Radiculoneuritis? Open Forum Infect Dis. 2016 Apr; 3(2): ofw085. Published online 2016 Apr 26. doi:  10.1093/ofid/ofw085

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He Got Schizophrenia. He Got Cancer. And Then He Got Cured.

He Got Schizophrenia. He Got Cancer. And Then He Got Cured.

A bone-marrow transplant treated a patient’s leukemia — and his delusions, too. Some doctors think they know why.
By Moises Velasquez-Manoff, science writer

CreditCreditJesse Jacobs

The man was 23 when the delusions came on. He became convinced that his thoughts were leaking out of his head and that other people could hear them. When he watched television, he thought the actors were signaling him, trying to communicate. He became irritable and anxious and couldn’t sleep.

Dr. Tsuyoshi Miyaoka, a psychiatrist treating him at the Shimane University School of Medicine in Japan, eventually diagnosed paranoid schizophrenia. He then prescribed a series of antipsychotic drugs. None helped. The man’s symptoms were, in medical parlance, “treatment resistant.”

A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

At first glance, the idea seems bizarre — what does the immune system have to do with the brain? — but it jibes with a growing body of literature suggesting that the immune system is involved in psychiatric disorders from depression to bipolar disorder.

The theory has a long, if somewhat overlooked, history. In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.
Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.
One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.
Modern doctors have also observed that people who suffer from certain autoimmune diseases, like lupus, can develop what looks like psychiatric illness. These symptoms probably result from the immune system attacking the central nervous system or from a more generalized inflammation that affects how the brain works.
Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.
Admittedly, these diseases are exceedingly rare, but their existence suggests there could be other immune disorders of the brain and nervous system we don’t know about yet.
Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance.
“The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past.

Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

Which brings us back to Dr. Miyaoka’s patient. There are other possible explanations for his recovery. Dr. Andrew McKeon, a neurologist at the Mayo Clinic in Rochester, Minn., a center of autoimmune neurology, points out that he could have suffered from a condition called paraneoplastic syndrome. That’s when a cancer patient’s immune system attacks a tumor — in this case, the leukemia — but because some molecule in the central nervous system happens to resemble one on the tumor, the immune system also attacks the brain, causing psychiatric or neurological problems. This condition was important historically because it pushed researchers to consider the immune system as a cause of neurological and psychiatric symptoms. Eventually they discovered that the immune system alone, unprompted by malignancy, could cause psychiatric symptoms.

Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia.

Once he had the same immune system, he developed similar psychiatric symptoms.

The bigger question is this: If so many syndromes can produce schizophrenia-like symptoms, should we examine more closely the entity we call schizophrenia?

Some psychiatrists long ago posited that many “schizophrenias” existed — different paths that led to what looked like one disorder. Perhaps one of those paths is autoinflammatory or autoimmune.

If this idea pans out, what can we do about it? Bone marrow transplant is an extreme and risky intervention, and even if the theoretical basis were completely sound — which it’s not yet — it’s unlikely to become a widespread treatment for psychiatric disorders. Dr. Yolken says that for now, doctors treating leukemia patients who also have psychiatric illnesses should monitor their psychiatric progress after transplantation, so that we can learn more.

And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

Dr. Yolken and colleagues recently explored this idea with a different tool: probiotics, microbes thought to improve immune function. He focused on patients with mania, which has a relatively clear immunological signal. During manic episodes, many patients have elevated levels of cytokines, molecules secreted by immune cells. He had 33 mania patients who’d previously been hospitalized take a probiotic prophylactically. Over 24 weeks, patients who took the probiotic (along with their usual medications) were 75 percent less likely to be admitted to the hospital for manic attacks compared with patients who didn’t.

The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.

Watershed moments occasionally come along in medical history when previously intractable or even deadly conditions suddenly become treatable or preventable. They are sometimes accompanied by a shift in how scientists understand the disorders in question.

We now seem to have reached such a threshold with certain rare autoimmune diseases of the brain. Not long ago, they could be a death sentence or warrant institutionalization. Now, with aggressive treatment directed at the immune system, patients can recover. Does this group encompass a larger chunk of psychiatric disorders? No one knows the answer yet, but it’s an exciting time to watch the question play out.

Moises Velasquez-Manoff, the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases” and an editor at Bay Nature magazine, is a contributing opinion writer.



This article is important on so many levels for Lyme/MSIDS patients as behavior/cognitive issues as well as immune-related issues are often present in those affected.  Killing pathogens is only one arm of treatment, that while important, is only part of the picture.  Detoxifying these pathogens as well as supporting the immune system is just as important.  Dealing with imbalances is a must.

Also noteworthy is the hyperthermia potential for Lyme/MSIDS as well as the impact of minocycline that while on it, schizophrenia patients completely normalized but when stopped their psychosis returned and how he prescribed the patients a low dose on a continuing basis.

Hmmmmm, the state medical board should come after him for overprescribing antibiotics….like they do Lyme doctors.

I personally found minocycline to be one of the most effective drugs I took.

Just for the record, I hate antibiotics, but they work.  I continue to be a human Guinea Pig and try many, many things, but nothing yet compares to antibiotics.  Recently an experienced Lyme practitioner in Wisconsin told me her patients do well off treatment for a year or two but then they suffer a relapse requiring a stint of antibiotics and/or herbs.  This has certainly been our experience as well.  

More on Mino:

More on the Immune system and schizophrenia:

Other brain abnormalities with Lyme/MSIDS:

BTW: t. gondii has been found in ticks (Ixodes ricinus), and these ticks also transmit Lyme and tick-borne encephalitis virus:, and  The story of Susannah Cahalan as well as the story of how a boy’s Lyme Disease Morphs into Autoimmune encephalopathy. It took 10 years and 20 doctors to find out 12-year-old Patrik had Lyme disease. Just 4 months later the doctors discovered he also has a condition where his immune system attacks his brain. “According to a Wisconsin specialist, 80% of his PANS/PANDAS patients have Lyme and other coinfections. This is important to know and tell others about, remembering that tick borne illness testing is abysmal. Getting to a specialist who understands this complexity is paramount. Another helpful tip is printing out and going through checklists with the children as discussing symptoms is quite helpful. Children aren’t experienced in this type of verbal specificity, so be patient and listen.


More Awareness Needed for Children’s Neurological Conditions

More awareness needed on children´s neurological conditions

Children who display sudden and severe personality and behavioural changes following a common illness such as strep throat could be suffering from neurological conditions rather than mental health issues, a charity has warned.

Paediatric Acute-onset Neuropsychiatric Syndrome (PANS) and Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) occurs when an infection triggers a misdirected immune response, resulting in brain inflammation.

This can lead the child to exhibit symptoms including anxiety, aggressive behaviour, depression and the onset of obsessive-compulsive disorder.

William Hewlett, who developed PANDAS at seven-years-old after catching chicken pox (PA/PANS PANDAS UK).


William Hewlett, who developed PANDAS at seven-years-old after catching chicken pox (PA/PANS PANDAS UK).

The conditions were first recognised in the United States in 1998 where it is estimated as many as one in 200 children could be affected, with the figure believed to be similar in the UK.

The charity PANS PANDAS UK said a failure to understand the condition in the UK means that children are regularly wrongly referred to Child and Adolescent Mental Health Services (CAMHS).

Treatments to address the underlying infection which causes the symptoms typically include a simple course of antibiotics.

Maya Humphries, from the West Midlands, has suffered from strep infections since she was a baby, but at the age of seven, following another bout of the infection, her family noticed a change in her behaviour overnight.

Her symptoms included Tourette’s, hallucinations, suicidal thoughts and separation anxiety, along with restricted eating and a fear of being sick.

The charity said GPs did not know how treat her and tried looking at each symptom in isolation, suggesting she had anorexia because she was not eating, and anxiety because she did not want to be left alone.

Frustrated with the lack of progress after four months, Maya and her family resorted to sitting in Birmingham Children’s Hospital until they agreed to give her an appointment with a neurologist.

She was found to have both PANS and PANDAS and her symptoms were settled with a course of long-term antibiotics.

However because of the delay in diagnosis and treatment Maya, now 10, still battles with the illness.

The charity has also helped William Hewlett, from Romsey, Hampshire, who developed PANDAS at seven-years-old after catching chicken pox.

His symptoms developed suddenly and included violent outbursts, hallucinations, not recognising his parents, avoiding food and trouble sleeping.

His frustrated family finally came to understand what was wrong with him after someone on a Facebook support group suggested they look into PANDAS.

They went on to request a prescription for antibiotics, and they saw drastic improvements within 24 hours.

Two private consultants have since diagnosed William, now eight, as having PANDAS but as no one on the NHS has come to the same conclusion, they are unable to pursue long-term treatment and so his family are now relying on homeopathy to manage his symptoms.

More than 200 medical professionals and families affected by the condition are expected to attend the first annual PANS PANDAS conference, which has been organised by the charity at Imperial College London on Saturday.

They will join the charity in calling for NHS England to support families affected by the condition and discuss options for raising awareness in the UK.

It said the World Health Organisation (WHO) has now acknowledged PANDAS but awareness needs to be raised in the UK too.

Chairwoman Georgia Tuckey said:

“Parents with children who have PANS or PANDAS regularly find themselves confused, helpless and desperate for someone to support their child.

“With better education in the medical community we can support these families faster and get their children on the long road to recovery quicker.”

Dr Andrew Curran, consultant paediatric neurologist at Alder Hey Children’s Hospital in Liverpool, said:

“It is essential that doctors should be alerted to the possibility of psychiatric and neurological disorder triggered by infections.

“With this knowledge an array of treatment options become available that can be transformative of a young person’s and their family’s lives.”

Vicky Burford, whose teenage boy has PANS, said:

“It was devastating to see our lovely son suddenly change.

“None of the diagnoses we were given seemed to fit his unique and strange combination of symptoms. Our son was disappearing before our eyes.

“My family suffered for two full years before getting appropriate treatment.

“No family deserves this, and we want to make sure that no other parent or child experiences the same nightmare.”



Please know that tick borne infections can also trigger this illness.  A prominent LLMD in Wisconsin states 80% of his PANS/PANDAS patients have underlying tick borne infections such as Lyme.

Notice that a simple course of antibiotics makes all the difference, but similarly to Lyme/MSIDS, if diagnosis and proper treatment is delayed, a person can struggle for years.

Since there are various triggers, some being viruses, antibiotics do not always work.

For more:



Connection Between ALS & Lyme?

Is there a connection between ALS and Lyme Disease?

Listen (Audio here)
By Tim Sandle     Jul 25, 2018 in Health
In the U.S. cases of Lyme Disease appear to be rising. Some researchers have drawn a link between the tick-transmitted bacterial infection and the neurodegenerative condition ALS. Jo Ann Simon explains more.
Screenshot_2018-09-21 Deer tick - Image - Digital Journal
Black legged Deer Tick – Jim Gathnany/CDC
According to the Center for Disease Control and Prevention, 376,000 cases of reported Lyme disease occur in the U.S. Lyme disease is a bacterial illness that can cause serious neurological problems. First discovered in the 1970s, Lyme disease draws its name from the Connecticut area, including the towns of Lyme and Old Lyme (see the Digital Journal article “Discoverer of Lyme disease dies”).

Lyme disease is difficult to detect until the symptoms, which arise in a person following the transfer of the pathogenic bacteria into the human blood stream as the result of a tick bite, appear.

The condition of amyotrophic lateral sclerosis (ALS), also known as motor neurone disease, received considerable attention a couple of years ago through the awareness campaign ‘Ice Bucket Challenge’. There are 20,000 people living with ALS at a given time, with 6,000 more being diagnosed in the U.S. every year.

Jo Ann Simon has been examining the connection between ALS and Lyme Disease based on her medical experiences and relevant statistics.

According to Simon,

“ALS, or amyotrophic lateral sclerosis, is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. A-myo-trophic comes from the Greek language. “A” means no. “Myo” refers to muscle, and “Trophic” means nourishment – “No muscle nourishment.”

She explains further:
“When a muscle has no nourishment, it “atrophies” or wastes away. “Lateral” identifies the areas in a person’s spinal cord where portions of the nerve cells that signal and control the muscles are located. As this area degenerates, it leads to scarring or hardening (“sclerosis”) in the region.”
Digital Journal: Is there a connection between Lyme Disease and ALS?

Jo Ann Simon: The culprit can be the spirochete borrelia burgodorferi bacteria of Lyme Disease or the unnamed foreign invader of ALS in the brain that triggers motor neuron disease, or are they the same?”

Our research, testing and discovery brought us through a maze of doctors, hospitals, treatments and various results. We celebrated when we thought it might be MMN Multi Focal Motor Neurothopy or Guilliane Barre, both treatable motor neuron diseases, but further testing eliminated that glimmer of hope.

DJ: What are the research highlights?

Simon: There are five little known facts about ALS and Lyme Disease, which research draws out. First, ALS and Lyme Disease have common ground with the auto immune and the central nervous systems. Second, common symptoms range from fatigue, numbness, muscle weakness and twitches, speech impairment, and cramping.

Third, recent studies that show that a significant percentage of ALS diagnosed patients test positive for Lyme Disease. Fourth, in some cases, patients diagnosed with ALS actually had Lyme Disease instead. And fifth, Lou Gehrig, the namesake of ALS lived very close to Lyme, Connecticut, where the disease was born.

DJ: What can people do to reduce the chance of infection?

Simon: The most important take away from this experience is that everyone needs to protect themselves, their family, friends and pets from ticks. Prevention of a tick bite could save your life! Prevention is the best medicine.

Also, use bug spray that has DEET (Off or Repel products) or Picaridin (Sawyer, Fisherman, Skin So Soft products). These are effective to deter ticks and can be found online, or at your local pharmacy, or department store.

If you are walking in grassy wooded areas, tuck in your pants to socks and wear long sleeve shirts so that your skin is not exposed. They might still jump on you for a ride, but you can eliminate them by running your clothes in a hot dryer for 10 minutes so they turn into harmless toast.

DJ: Is there anything else?

Simon: Yes, you can treat your shoes and clothes with Permithrin, a synthetic pesticide that repels ticks from 5 to 70 washes, depending on the product. Insect Shield in North Carolina will treat your clothes for up to 70 washes, or you can treat yourself with different products such as Sawyer insect repellent which can be purchased on line or at your local pharmacy, grocery or department store. L.L. Bean and Cabela’s sell pretreated clothes and camping gear.

Protect your pet. If you stopped your pet’s tick preventive over the winter, get it started again now. Outdoor dogs and cats will likely be the first family members to find a tick and bring it home to you. There are two types of products to use. Products that kill ticks on contact – quick tick gone or kill ticks after their lunch – bite to die. Talk to your vet to decide the best product for your pet.

Also, get professional treatment for your property to eliminate the threat of ticks in your outside living areas. This does not stop the threat elsewhere, but at least you can sleep at night not worrying about the ticks on your doorstep. Do a tick check every day. This is especially important for your children and pets since they normally spend the most time outside.


For More:    She found that Lyme was likely the cause of her deterioration in health, got treated for it and stopped the progression of the ‘ALS’. She’s still alive now, although hardly after the damage the original documentary had done to her care plan. years of medical observations that some people with amyotrophic lateral sclerosis — better known as Lou Gehrig’s disease, or ALS — also suffer from a form of dementia. Conversely, some patients with dementia also have been observed developing crippling symptoms similar to those in ALS, where patients gradually lose control of their muscles.  This latest common protein discovery in a way adds another link in the chain of research into the major neurodegenerative diseases. Now, a faulty protein has been uncovered in Alzheimer’s, Parkinson’s and Huntington’s diseases, among others. Each of these diseases remains incurable, but scientists believe discoveries such as this represent a major step forward in finding a cure.

A relationship between ALS / MND (motor neuron disease) and Lyme makes sense, looking at the findings of the 1990 research that was published in the article ‘Immunological Reactivity against in Borrelia burgdorferi in Patients with Motor Neuron Disease’ by Halperin et al.  This study showed that in almost 50% of the 19 people diagnosed with ALS, Lyme was the cause. Once treated, several of these patients improved. In that same year, 1990, the CDC published its first definition about Lyme and described the complex, systemic, multi-symptom and sometimes devastating chronic disease experienced by many Lyme patients – then and still today.

Did anyone ever do a follow-up on this promising research? No. It was simply hidden away and Halperin chose to become a co-author of the 2006 IDSA Lyme Guidelines instead, which maintain that ‘Lyme is a mild disease that is hard to get, easy to treat and hardly ever becomes a chronic condition’. Any possible connection with ALS or any other of the serious and previously acknowledged debilitating or even deadly conditions was no longer mentioned. Any long-term health issues are reasoned away, using semantics rather than ‘evidence based’ science.  Watch parts 1 & 4 to see how Lyme can masquerade as other neurodegenerative illnesses.

And lastly, if you want to see first-hand a doctor (Dr. Martz) diagnosed with ALS who got his life back after Lyme was discovered & treated, watch the excellent documentary, “Under Our Skin.”  Story here:

You can also read about Dr. Martz in “Cure Unknown: Inside the Lyme Epidemic,” by Pamela Weintraub.

Underlying Infections & Psychiatric Presentation – Podcast

Episode 38: Underlying Infections and Psychiatric Presentation

Cindy Kennedy, FNP, is joined by Dr. Rosalie Greenberg, who discusses how underlying infections can manifest themselves with a psychiatric presentation, particularly among children with Lyme disease.

Greenberg, D.F.A.A.C.A.P., is a Board Certified Child and Adolescent Psychiatrist in private practice in New Jersey. She specializes in the diagnosis and psychopharmacological treatment of Pediatric Mood Disorders, psychiatric symptoms secondary to tick-borne infections and Pediatric Acute-onset Neuropsychiatric Syndromes.
She is an active member of The International Lyme and Associated Diseases Society (ILADS) and has authored articles and lectured at ILADS National and International Conferences on Tick-borne Illnesses and Childhood Psychiatric Symptoms.
In addition Dr. Greenberg is the author of “Bipolar Kids: Helping your Child Find Calm in the Mood Storm,” DaCapo Press (March 2007), co-producer of the film: Rescuing Childhood- Understanding Bipolar Disorders in Children and Adolescents (2009); host of The Telly Award winning show “Kids First with Rosalie Greenberg, MD” (2012, 2013, 2014, 2015), and recipient of multiple awards and acknowledgement as a Top Doctor in several publications. She maintains a private practice in Summit, New Jersey.