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:



1.) Garin-Bujadoux C: Paralysie par les tiques. J Med Lyon 3:765-767, 1922

2.) Afzelius A: Erythema chronicum migrans. Acta Derm Venereol 2:120-125, 1921

3.) Hellerstrom S: Erythema chronicum migrans Afzelii. Acta Derm Venereol 11:315-321, 1930

4.) Bannwarth A: Chronische lymphocytare Meningitis, entzundliche Polyneuritis und “Rheumatismus.” Ein Beitrag zum Problem “Allergie und Nervensystem.” Arch Psychiat Nervenkr 113:284-376,1941

5.) Bannwarth A: Zur Klinik und Pathogenese der “chronischen lymphocytaren Meningitis.” Arch Psychiat Nervenkr 117:161-185, 1944

6.) Bannwarth A: Zur Klinik und Pathogenese der “chronischen lymphocytaren Meningitis.” Arch Psychiat Nervenkr 117:682-716, 1944.

7.) Binder, E., R. Doepfmer, et al. (1955). ”[Experimental transmission  of  chronic  erythema  migrans  from man to man.].” Hautarzt 6(11): 494-6

8.) Lefevre JP, Pouget-Abadie JF, Bontoux D, Sudre Y, Gil R. [Meningoradiculitis after tick bites. Apropos of 9 cases]. Sem Hop. 1976 Mar 16;52(11):687-94. [Article in French]

9.) Goffinet AM, Laterre C. [Tick-bite meningoradiculitis (author’s transl)]. Acta Neurol Belg. 1978 Jul-Aug;78(4):217-22. [Article in French]

10.) Burgdorfer,  W., A.  G.  Barbour,  et  al.  (1982).  “Lyme disease-a    tick-borne    spirochetosis?” Science 216(4552): 1317-9.

11.) Burgdorfer W.How the discovery of Borrelia burgdorferi came about. Clin Dermatol. 1993 Jul-Sep;11(3):335-8.

12.) Hindfelt B, Jeppsson PG, Nilsson B, et al: Clinical and cerebrospinal fluid findings in lymphocytic meningoradiculitis (Bannwarth’s syndrome). Acta Neurol Scandinav 66:444-453, 1982,

13.) Skoldenberg B, Stiernstedt G, Garde A, et al: Chronic meningitis caused by a penicillin-sensitive microorganism? Lancet ii:75-78, 1983

14.) Pachner AR, Steere AC. Neurological findings of Lyme disease. Yale J Biol Med. 1984 Jul-Aug;57(4):481-3.

15.) Pfister HW, Einhäupl K, Preac-Mursic V, Wilske B, Schierz G. The spirochetal etiology of lymphocytic meningoradiculitis of Bannwarth (Bannwarth’s syndrome). J Neurol. 1984;231(3):141-4.

16.) Ryberg B. Bannwarth’s syndrome (lymphocytic meningoradiculitis) in Sweden. Yale J Biol Med. 1984 Jul-Aug;57(4):499-503.

17.) Weber K. [Jarisch-Herxheimer reaction in erythema migrans disease].[Article in German]Hautarzt. 1984 Nov;35(11):588-90.

18.) Jarisch A (1895). “Therapeutische Versuche bei Syphilis”. Wien Med Wochenschr. 45: 721–42.

19.) Herxheimer K, Krause D (1902). “Ueber eine bei Syphilitischen vorkommende Quecksilberreaktion”. Deutsch Med Wochenschr. 28 (50): 895–7. doi:10.1055/s-0028-1139096.

20.) Bowen GS, Griffin M, Hayne C, Slade J, Schulze TL, Parkin W. Clinical manifestations and descriptive epidemiology of Lyme disease in New Jersey, 1978 to 1982. JAMA. 1984 May 4;251(17):2236-40.

21.) Christen HJ, Delekat D, Rating D, Hanefeld F.[Erythema migrans disease. 3 case examples with neurologic complications].[Article in German]. Monatsschr Kinderheilkd. 1985 Oct;133(10):732-7.

22.) Stiernstedt GT, Granström M, Hederstedt B, Sköldenberg B. Diagnosis of spirochetal meningitis by enzyme-linked immunosorbent assay and indirect immunofluorescence assay in serum and cerebrospinal fluid. J Clin Microbiol. 1985 May;21(5):819-25.

23.) MacDonald AB. Borrelia in the brains of patients dying with dementia. JAMA. 1986 Oct 24-31;256(16):2195-6.

24.) Reik L Jr, Burgdorfer W, Donaldson JO. Neurologic abnormalities in Lyme disease without erythema chronicum migrans. Am J Med. 1986 Jul;81(1):73-8.

25.) MacDonald AB, Miranda JM. Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987 Jul;18(7):759-61.

26.) Pfister HW, Einhäupl KM, Wilske B, Preac-Mursic V. Bannwarth’s syndrome and the enlarged neurological spectrum of arthropod-borne borreliosis. Zentralbl Bakteriol Mikrobiol Hyg A. 1987 Feb;263(3):343-7.

27.) Hofstad H, Matre R, Nyland H, Ulvestad E. Bannwarth’s syndrome: serum and CSF IgG antibodies against Borrelia burgdorferi examined by ELISA. Acta Neurol Scand. 1987 Jan;75(1):37-45.

28.) C J Sindic, A Depre, G Bigaignon, P F Goubau, P Hella, and C Laterre. Lymphocytic meningoradiculitis and encephalomyelitis due to Borrelia burgdorferi: a clinical and serological study of 18 cases. J Neurol Neurosurg Psychiatry. 1987 Dec; 50(12): 1565–1571.

29.) Hirsch E, Sellal F, Christmann D, Steinmetz G, Monteil H, Jesel M, Warter JM, Collard M. [Meningoradiculitis after a tick bite. Study of 31 cases]. Rev Neurol (Paris). 1987;143(3):182-8. [Article in French]

30.) Lubeau M, Vallat JM, Hugon J, Dumas M, Desproges-Gotteron R. Tick bite meningoradiculitis. Ten cases. Zentralbl Bakteriol Mikrobiol Hyg A. 1987 Feb;263(3):321-3.

31.) Masson C. [Neurologic aspects of Lyme disease]. Presse Med. 1987 Jan 24;16(2):72-5.[Article in French]

32.) Moore JA. Jarisch-Herxheimer reaction in Lyme disease. Cutis. 1987 May;39(5):397-8.

33.) Dupuis MJ.[Multiple neurologic manifestations of Borrelia burgdorferi infection]. Rev Neurol (Paris). 1988;144(12):765-75. [Article in French]

34.) Pachner AR. Neurologic manifestations of Lyme disease, the new “great imitator”. Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1482-6.

35.) Kristoferitsch W1. Lyme borreliosis in Europe. Neurologic disorders. Rheum Dis Clin North Am. 1989 Nov;15(4):767-74.

36.) Pizzarello LD1, MacDonald AB, Semlear R, DiLeo F, Berger B. Temporal arteritis associated with Borrelia infection. A case report. J Clin Neuroophthalmol. 1989 Mar;9(1):3-6.

37.) Bialasiewicz AA, Huk W, Druschky KF, Naumann GO.[Borrelia burgdorferi infection with bilateral optic neuritis and intracerebral demyelinization lesions].[Article in German] Klin Monbl Augenheilkd. 1989 Aug;195(2):91-4.

38.) Meier C, Grahmann F, Engelhardt A, Dumas M. Peripheral nerve disorders in Lyme-Borreliosis. Nerve biopsy studies from eight cases. Acta Neuropathol. 1989;79(3):271-8.

39.) Miklossy J1, Kuntzer T, Bogousslavsky J, Regli F, Janzer RC. Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis. Acta Neuropathol. 1990;80(5):568-72.

40.) Kohler J. [Lyme borreliosis in neurology and psychiatry]. Fortschr Med. 1990 Apr 10;108(10):191-3, 197. [Article in German]

41.) Kristoferitsch W. Neurological manifestations of Lyme borreliosis: clinical definition and differential diagnosis. Scand J Infect Dis Suppl. 1991;77:64-73.

42.) Krupp, L.B.; Masur, D.; Schwartz, J.; Coyle, P.K.; Langenbach, L.J.; Fernquist, S.K.; Jandorf, L.; Halperin, J.J. Cognitive functioning in late Lyme borreliosis. Arch. Neurol. 1991, 48, 1125–1129.

43.) Kaplan, R.F.; Meadows, M.E.; Vincent, L.C.; Logigian, E.L.; Steere, A.C. Memory impairment and depression in patients with Lyme encephalopathy: Comparison with fibromyalgia and nonpsychotically depressed patients. Neurology 1992, 42, 1263–1267.

44.) Fallon BA1, Nields JA, Parsons B, Liebowitz MR, Klein DF. Psychiatric manifestations of Lyme borreliosis. J Clin Psychiatry. 1993 Jul;54(7):263-8.

45.)  Kalish RA1, Leong JM, Steere AC. Association of treatment-resistant chronic Lyme arthritis with HLA-DR4 and antibody reactivity to OspA and OspB of Borrelia burgdorferi. Infect Immun. 1993 Jul;61(7):2774-9.

46.) Fallon, B.A.; Nields, J.A. Lyme disease: A neuropsychiatric illness. Am. J. Psychiatry 1994, 151, 1571–1583.

47.) García Moncó JC1, Wheeler CM, Benach JL, Furie RA, Lukehart SA, Stanek G, Steere AC.Reactivity of neuroborreliosis patients (Lyme disease) to cardiolipin and gangliosides. J Neurol Sci. 1993 Jul;117(1-2):206-14.

48.) Schaeffer S, Le Doze F, De la Sayette V, Bertran F, Viader F. [Dementia in Lyme disease]. Presse Med. 1994 May 14;23(18):861. [Article in French]

49.) Waniek C1, Prohovnik I, Kaufman MA, Dwork AJ. Rapidly progressive frontal-type dementia associated with Lyme disease. J Neuropsychiatry Clin Neurosci. 1995 Summer;7(3):345-7.

50.) Benke, T.; Gasse, T.; Hittmair-Delazer, M.; Schmutzhard, E. Lyme encephalopathy: Long-term neuropsychological deficits years after acute neuroborreliosis. Acta Neurol. Scand. 1995, 91, 353–357.

51.) Garcia-Monco JC1, Benach JL. Lyme neuroborreliosis. Ann Neurol. 1995 Jun;37(6):691-702.

52.) Stein, S.L.; Solvason, H.B.; Biggart, E.; Spiegel, D. A 25-year-old woman with hallucinations, hypersexuality, nightmares, and a rash. Am. J. Psychiatry 1996, 153, 545–551.

53.) Garcia-Monco JC1, Benach JL.. Mechanisms of injury in Lyme neuroborreliosis. Semin Neurol. 1997 Mar;17(1):57-62.

54.) Kaplan, R.F.; Jones-Woodward, L. Lyme encephalopathy: A neuropsychological perspective. Semin. Neurol. 1997, 17, 31–37.

55.) Gaudino EA, Coyle PK, Krupp LB. Post-Lyme syndrome and chronic fatigue syndrome. Neuropsychiatric similarities and differences. Arch Neurol. 1997 Nov;54(11):1372-6.

56.) Maloy AL1, Black RD, Segurola RJ Jr. Lyme disease complicated by the Jarisch-Herxheimer reaction. J Emerg Med. 1998 May-Jun;16(3):437-8.

57.) Arteaga F1, García-Moncó JC[Association of Lyme disease with work and leisure activities].  Enferm Infecc Microbiol Clin. 1998 Jun-Jul;16(6):265-8. [Article in Spanish]

58.) Schmitt AB1, Küker W, Nacimiento W. [Neuroborreliosis with extensive cerebral vasculitis and multiple cerebral infarcts]. Nervenarzt. 1999 Feb;70(2):167-71. [Article in German]

59.) Kaplan, R.F.; Jones-Woodward, L.; Workman, K.; Steere, A.C.; Logigian, E.L.; Meadows, M.E. Neuropsychological deficits in Lyme disease patients with and without other evidence of central nervous system pathology. Appl. Neuropsychol. 1999, 6, 3–11.

60.) Sherr, V.T. Panic attacks may reveal previously unsuspected chronic disseminated Lyme disease. J. Psychiatr. Pract. 2000, 6, 352–356.

61.) Elkins LE, Pollina DA, Scheffer SR, Krupp LB. Psychological states and neuropsychological performances in chronic Lyme disease. Appl Neuropsychol. 1999;6(1):19-26.

62.) Diagnostic Tests for Borrelia – Lyme/TBRF 1.991-2.018

63.) Rudnik-Szałaj I1, Popławska R, Zajkowska J, Szulc A, Pancewicz SA, Gudel I. [Mental disorders in Lyme disease].  Pol Merkur Lekarski. 2001 Nov;11(65):460-2. [Article in Polish]

64.) Seijo Martínez M1, Grandes Ibáñez J, Sánchez Herrero J, García-Moncó JC. Spontaneous brain hemorrhage associated with Lyme neuroborreliosis. Neurologia. 2001 Jan;16(1):43-5.

65.) Gutiérrez MA1, de Pablos C, Oterino A, García Moncó JC.[Isolated posterior cord syndrome in Lyme s disease: a clinico neurophysiological study]. Rev Neurol. 2001 Nov 16-30;33(10):954-7. [Article in Spanish]

66.) Tager, F.A.; Fallon, B.A.; Keilp, J.; Rissenberg, M.; Jones, C.R.; Liebowitz, M.R. A controlled study of cognitive deficits in children with chronic Lyme disease. J. Neuropsychiatry Clin. Neurosci. 2001, 13, 500–507.

67.) Gustaw, K.; Beltowska, K.; Studzinska, M.M. Neurological and psychological symptoms after the severe acute neuroborreliosis. Ann. Agric. Environ. Med. 2001, 8, 91–94.

68.) Kovalchuka L1, Eglite J, Lucenko I, Zalite M, Viksna L, Krumiņa A. Associations of HLA DR and DQ molecules with Lyme borreliosis in Latvian patients. BMC Res Notes. 2012 Aug 14;5:438. doi: 10.1186/1756-0500-5-438.

69.) Hájek, T.; Pasková, B.; Janovská, D.; Bahbouh, R.; Hájek, P.; Libiger, J.; Höschl, C. Higher prevalence of antibodies to Borrelia burgdorferi in psychiatric patients than in healthy subjects. Am. J. Psychiatry 2002, 159, 297–301.

70.) Schneider, R.K.; Robinson, M.J.; Levenson, J.L. Psychiatric presentations of non-HIV infectious diseases. Neurocysticercosis, Lyme disease, and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection. Psychiatr. Clin. N. Am. 2002, 25, 1–16.

71.)Westervelt HJ, McCaffrey RJ. Neuropsychological functioning in chronic Lyme disease. Neuropsychol Rev. 2002 Sep;12(3):153-77.

72.) Cassarino DS, Quezado MM, Ghatak NR, Duray PH. Lyme-associated parkinsonism: a neuropathologic case study and review of the literature. Arch Pathol Lab Med. 2003;127(9):1204-6.

73.) Stricker, R.B.; Winger, E.E. Musical hallucinations in patients with Lyme disease. South Med. J. 2003, 96, 711–715.

74.) Bär, K.J.; Jochum, T.; Häger, F.; Meissner, W.; Sauer, H. Painful hallucinations and somatic delusions in a patient with the possible diagnosis of neuroborreliosis. Clin. J. Pain 2005, 21, 362–363.

75.)  Iliopoulou BP1, Guerau-de-Arellano M, Huber BT. HLA-DR alleles determine responsiveness to Borrelia burgdorferi antigens in a mouse model of self-perpetuating arthritis. Arthritis Rheum. 2009 Dec;60(12):3831-40. doi: 10.1002/art.25005.

76.) Jones CR, Smith H, Gibb E, Johnson L (2005) Gestational Lyme Disease: Case Studies of 102 Live Births. Lyme Times. Gestational Lyme Studies 34-36

77.) Almeida OP1, Lautenschlager NT. Dementia associated with infectious diseases. Int Psychogeriatr. 2005;17 Suppl 1:S65-77.

78.) Keilp, J.G.; Corbera, K.; Slavov, I.; Taylor, M.J.; Sackeim, H.A.; Fallon, B.A. WAIS-III and WMS-III performance in chronic Lyme disease. J. Int. Neuropsychol. Soc. 2006, 12, 119–129.

79.) MacDonald, A.B. Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete. Med. Hypotheses 2006, 67, 592–600.

80.)  Steere AC1, Klitz W, Drouin EE, Falk BA, Kwok WW, Nepom GT, Baxter-Lowe LA. Antibiotic-refractory Lyme arthritis is associated with HLA-DR molecules that bind a Borrelia  burgdorferi peptide. J Exp Med. 2006 Apr 17;203(4):961-71. Epub 2006 Apr 3.

81.) MacDonald AB. Alzheimer’s neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes. Med Hypotheses. 2007;68(4):822-5. Epub 2006 Oct 20.

82.) Czupryna P1, Kusmierczyk J, Zajkowska JM, Ciemerych M, Kondrusik M, Ciemerych A, Pancewicz SA. [Clinical forms of neuroborreliosis among hospitalized patients in the years 2000-2005].[Article in Polish] Pol Merkur Lekarski. 2007 Aug;23(134):103-6.

83.) Bransfield, R.C. Lyme Disease, comorbid tick-borne diseases, and neuropsychiatric disorders. Psychiatr. Times 2007, 24, 59–61.

84.) Scheffer, R.E.; Linden, S. Concurrent medical conditions with pediatric bipolar disorder. Curr. Opin. Psychiatry 2007, 20, 398–401.

85.) Habek M1, Mubrin Z, Brinar VV. Avellis syndrome due to borreliosis. Eur J Neurol. 2007 Jan;14(1):112-4.

86.) Schweighofer CD1, Fätkenheuer G, Staib P, Hallek M, Reiser M. Lyme disease in a patient with chronic lymphocytic leukemia mimics leukemic meningeosis. Onkologie. 2007 Nov;30(11):564-6. Epub 2007 Oct 16.

87.) Miklossy J. Chronic inflammation and amyloidogenesis in Alzheimer’s disease — role of Spirochetes. J Alzheimers Dis. 2008 May;13(4):381-91.

88.) Miklossy J1. Biology and neuropathology of dementia in syphilis and Lyme disease. Handb Clin Neurol. 2008;89:825-44. doi: 10.1016/S0072-9752(07)01272-9.

89.) Fallon, B.A.; Keilp, J.G.; Corbera, K.M.; Petkova, E.; Britton, C.B.; Dwyer, E.; Slavov, I.; Cheng, J.; Dobkin, J.; Nelson, D.R.; et al. A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy. Neurology 2008, 70, 992–1003.

90.) Bransfield, R.C. Lyme Disease and Cognitive Impairments. Science Research, 8 August 2008. Available online:

91.) Hassett, A.L.; Radvanski, D.C.; Buyske, S.; Savage, S.V.; Gara, M.; Escobar, J.I.; Sigal, L.H. Role of psychiatric comorbidity in chronic Lyme disease. Arthritis Rheum. 2008, 59, 1742–1749.

92.) Helon B1, Tłuczek TW, Buczyjan A, Adamczyk-Helon A, Wojnarowicz M, Mikuła R, Ciciński P, Bojarska. [Polymorphic mental disorders in the course of Lyme borreliosis–case study]. Psychiatr Pol. 2009 May-Jun;43(3):353-61 [Article in Polish]

93.) Bransfield, R.C.; Wulfman, J.S.; Harvey, W.T.; Usman, A.I. The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders. Med. Hypotheses 2008, 70, 967–974.

94.) Vojdani, A. Antibodies as predictors of complex autoimmune diseases and cancer. Int. J. Immunopathol. Pharmacol. 2008, 21, 553–566.

95.) Bransfield, R.C. Preventable cases of autism: Relationship between chronic infectious diseases and neurological outcome. Pediatr. Health 2009, 3, 125–140.

96.) Nicolson, G.; Haier, J. Role of Chronic bacterial and viral infections in neurodegenerative, neurobehavioral, psychiatric, autoimmune and fatiguing illnesses: Part 1. BJMP 2009, 2, 20–28.

97.)Parish, J.M. Sleep-related problems in common medical conditions. Chest 2009, 135, 563–572.

98.) Nafeev AA, Klimova LV. [Clinical manifestations of neuroborreliosis in the Volga region]. Ter Arkh. 2010;82(11):68-70. [Article in Russian]

99.) .) Steffen, A.; Hagenah, J.; Wollenberg, B.; Brüggemann, N. A case of central sleep apnea strictly dependent upon REM-sleep. J. Neurol. 2010, 257, 143–145.

100.) Polat, E.; Turhan, V.; Aslan, M.; Müsellim, B.; Onem, Y.; Ertugrul, B. First report of three culture confirmed human Lyme cases in Turkey. Mikrobiyol. Bul. 2010, 44, 133–139.

101.) McAuliffe, P.; Brassard, M.R.; Fallon, B. Memory and Executive Functions in Adolescents with Posttreatment Lyme Disease. Appl. Neuropsychol. 2010, 15, 208–219.

102.) Stricker, R.B.; Johnson, L. Lyme disease diagnosis and treatment: Lessons from the AIDS epidemic. Minerva Med. 2010,

103.) Fallon, B.A.; Levin, E.S.; Schweitzer, P.J.; Hardesty, D. Inflammation and central nervous system Lyme disease. Neurobiol. Dis. 2010, 37, 534–541

104.) Markeljevic, J.; Sarac, H.; Rados, M. Tremor, seizures and psychosis as presenting symptoms in a patient with chronic Lyme neuroborreliosis (LNB). Coll. Antropol. 2011, 35, 313–318.

105.) 18. Michel JM1, Sellal F. [“Reversible” dementia in 2011]. Geriatr Psychol Neuropsychiatr Vieil. 2011 Jun;9(2):211-25. doi: 10.1684/pnv.2011.0274.

106.) Gheorghiev, C.; De Montleau, F.; Defuentes, G. Alcohol and epilepsy: A case report between alcohol withdrawal seizures and neuroborreliosis. Encephale 2011, 37, 231–237.

107.) Miklossy, J. Alzheimer’s disease—A neurospirochetosis. Analysis of the evidence following Koch’s and Hill’s criteria. J. Neuroinflamm. 2011, 8, 90.

108.) Lyme Disease (Borrelia burgdorferi) 2011 Case Definition CSTE Position Statement(s) 10-ID-06. CDC, 2011. Available online: (accessed on 30 August 2018).

109.) Schutzer, S.E.; Angel, T.E.; Liu, T.; Schepmoes, A.A.; Clauss, T.R.; Adkins, J.N.; Camp, D.G.; Holland, B.K.; Bergquist, J.; Coyle, P.K.; et al. Distinct cerebrospinal fluid proteomes differentiate post-treatment Lyme disease from chronic fatigue syndrome. PLoS ONE 2011, 6, e17287.

110.) Stricker, R.B.; Delong, A.K.; Green, C.L.; Savely, V.R.; Chamallas, S.N.; Johnson, L. Benefit of intravenous antibiotic therapy in patients referred for treatment of neurologic Lyme disease. Int. J. Gen. Med. 2011, 4, 639–646.

111.) Rhee, H.; Cameron, D.J. Lyme disease and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS): An overview. Int. J. Gen. Med. 2012, 5, 163–174.

112.) Miklossy J1. Chronic or late lyme neuroborreliosis: analysis of evidence compared to chronic or late neurosyphilis. Open Neurol J. 2012;6:146-57. doi: 10.2174/1874205X01206010146. Epub 2012 Dec 28.

113.) Miklossy, J.; Donta, S.; Mueller, K.; Nolte, O.; Perry, G. Chronic or late Lyme neuroborreliosis: Present and future. Open Neurol. J. 2012, 6, 78.

114.) Hastey, C.J.; Elsner, R.A.; Barthold, S.W.; Baumgarth, N. Delays and diversions mark the development of B cell responses to Borrelia burgdorferi infection. J. Immunol. 2012, 188, 5612–5622.

115.) Bransfield, R.C. The psychoimmunology of Lyme/Tick-Borne diseases and its association with neuropsychiatric symptoms. Open Neurol. J. 2012, 688–693.

116.) Bransfield, R.C. Inflammation and autoimmunity in Lyme disease and psychiatric sequellae. Psychiatr. Ann. 2012, 42, 337–341.

117.) Kuhn, M.; Grave, S.; Bransfield, R.; Harris, S. Long term antibiotic therapy may be an effective treatment for children co-morbid with Lyme disease and autism spectrum disorder. Med. Hypotheses 2012, 78, 606–615.

118.) Kovalchuka L1, Eglite J, Lucenko I, Zalite M, Viksna L, Krumiņa A. Associations of HLA DR and DQ molecules with Lyme borreliosis in Latvian patients. BMC Res Notes. 2012 Aug 14;5:438. doi: 10.1186/1756-0500-5-438.

119.) Klempner MS1, Baker PJ, Shapiro ED, Marques A, Dattwyler RJ, Halperin JJ, Wormser GP. Treatment trials for post-Lyme disease symptoms revisited. Am J Med. 2013 Aug;126(8):665-9. doi: 10.1016/j.amjmed.2013.02.014. Epub 2013 Jun 10.

120.) Kuehn, B.M. CDC estimates 300,000 US cases of Lyme disease annually. JAMA 2013, 310, 1110.

121.) Chung, Y.; Zhang, N.; Wooten, R.M. Borrelia burgdorferi elicited-IL-10 suppresses the production of inflammatory mediators, phagocytosis, and expression of co-stimulatory receptors by murine macrophages and/or dendritic cells. PLoS ONE 2013, 8, e84980.

122.) Berndtson, K. Review of evidence for immune evasion and persistent infection in Lyme disease. Int. J. Gen. Med. 2013, 6, 291–306.

123.) Back, T.; Grünig, S.; Winter, Y.; Bodechtel, U.; Guthke, K.; Khati, D.; von Kummer, R. Neuroborreliosis-associated cerebral vasculitis: Long-term outcome and health-related quality of life. J. Neurol. 2013, 260, 1569–1575.

124.) Ajamian, M.; Rajadhyaksha, A.M.; Alaedini, A. Autism and Lyme disease—Reply. JAMA 2013, 310, 857.

125.) Bransfield, R.C.; Kuhn, M. Autism and Lyme disease. JAMA 2013, 310, 856–857.

126.) Aucott, J.N.; Rebman, A.W.; Crowder, L.A.; Kortte, K.B. Post-treatment Lyme disease syndrome symptomatology and the impact on life functioning: Is there something here? Qual. Life Res. 2013, 22, 75–84.

127.) Shea, L. Psychological symptoms in children with Lyme Disease. In Proceedings of the Challenges and Controversy in Lyme Disease and Tick-Borne Illness Care Symposium, Massachusetts General Hospital, Boston, MA, USA, 9 November 2013.

128.) 1.) Blanc F1, Philippi N1, Cretin B1, Kleitz C2, Berly L2, Jung B1, Kremer S3, Namer IJ4, Sellal F5, Jaulhac B6, de Seze J7. Lyme neuroborreliosis and dementia. J Alzheimers Dis. 2014;41(4):1087-93. doi: 10.3233/JAD-130446.

129.) Hinckley, A.F.; Connally, N.P.; Meek, J.I.; Johnson, B.J.; Kemperman, M.M.; Feldman, K.A.; White, J.L.; Mead, P.S. Lyme disease testing by large commercial laboratories in the United States. Clin. Infect. Dis. 2014, 59, 676–681.

130.) Kuhn, M.; Bransfield, R. Divergent opinions of proper Lyme disease diagnosis and implications for children co-morbid with autism spectrum disorder. Med. Hypotheses 2014, 83, 321–325.

131.) Johnson, L.; Wilcox, S.; Mankoff, J.; Stricker, R.B. Severity of chronic Lyme disease compared to other chronic conditions: A quality of life survey. PeerJ 2014, 2, e322.

132.) Bransfield, R.C. Sleep disorders impacting Lyme patients. In Proceedings of the 15th Annual ILADS Scientific Conference, Washington, DC, USA, 10 October 2014.

133.) Lobraico, J.; Butler, A.; Petrini, J.; Ahmadi, R. New insights into stages of Lyme disease symptoms from a novel hospital-based registry. J. Prim. Care Community Health 2014, 5, 284–287.

134.) Zimering, J.H.; Williams, M.R.; Eiras, M.E.; Fallon, B.A.; Logigian, E.L.; Dworkin, R.H. Acute and chronic pain associated with Lyme borreliosis: Clinical characteristics and pathophysiologic mechanisms. Pain 2014, 155, 1435–1438.

135.)  Miklossy J. Historic evidence to support a causal relationship between spirochetal infections and Alzheimer’s disease. Front Aging Neurosci. 2015 Apr 16;7:46. doi: 10.3389/fnagi.2015.00046. eCollection 2015.

136.) Scieszka J1, Dabek J2, Cieslik P1. Post-Lyme disease syndrome. Reumatologia. 2015;53(1):46-8. doi: 10.5114/reum.2015.50557. Epub 2015 Apr 10.

137.) Marques AR. Lyme Neuroborreliosis. Continuum (Minneap Minn). 2015 Dec;21(6 Neuroinfectious Disease):1729-44. doi: 10.1212/CON.0000000000000252.

138.) Kadam P1, Gregory NA, Zelger B, Carlson JA. Delayed onset of the Jarisch-Herxheimer reaction in doxycycline-treated disease: a case report and review of its histopathology and implications for pathogenesis. Am J Dermatopathol. 2015 Jun;37(6):e68-74. doi: 10.1097/DAD.0000000000000093.

139.) Lesourd A1, Ngo S1, Sauvêtre G1, Héron F1, Levesque H1, Marie I2.[Facial diplegia as the presenting feature of Lyme disease].[Article in French] Rev Med Interne. 2015 May;36(5):352-5. doi: 10.1016/j.revmed.2014.05.002. Epub 2014 Aug 2

140.) Forrester, J.D.; Kugeler, K.J.; Perea, A.E.; Pastula, D.M.; Mead, P.S. No Geographic Correlation between Lyme Disease and Death Due to 4 Neurodegenerative Disorders, United States, 2001–2010. Emerg. Infect. Dis. 2015, 21, 2036–2039.

141.) Wormser, G.P.; Weitzner, E.; McKenna, D.; Nadelman, R.B.; Scavarda, C.; Molla, I.; Dornbush, R.; Visintainer, P.; Nowakowski, J. Long-term assessment of health-related quality of life in patients with culture-confirmed early Lyme disease. Clin. Infect. Dis. 2015, 61, 244–247.

142.) Greenberg, R. Study design questions regarding long-term assessment of health-related quality of life in patients with culture-confirmed early Lyme disease. Clin. Infect. Dis. 2015, 61, 1764–1765.

143.) Smith, A.; Oertle, J.; Warren, D.; Prato, D. Chronic Lyme disease complex and its commonly undiagnosed primary and secondary co-infections. Open J. Med. Microbiol. 2015, 5, 143–158.

144.) Bransfield, R.C. List of 700 Articles Citing Chronic Infection Associated with Tick-Borne Diseases Compiled by Dr. Robert Bransfield. ILADS, 2015. Available online: (accessed on 30 august 2018).

145.) Nelson, C.A.; Saha, S.; Kugeler, K.J.; Delorey, M.J.; Shankar, M.B.; Hinckley, A.F.; Mead, P.S. Incidence of clinician-diagnosed Lyme disease, United States, 2005–2010. Emerg. Infect. Dis. 2015, 21, 1625–1631.

146.) 31.)Kadam P1, Gregory NA, Zelger B, Carlson JA.  Delayed onset of the Jarisch-Herxheimer reaction in doxycycline-treated disease: a case report and review of its histopathology and implications for pathogenesis. Am J Dermatopathol. 2015 Jun;37(6):e68-74. doi: 10.1097/DAD.0000000000000093.

147.) Lesourd A1, Ngo S1, Sauvêtre G1, Héron F1, Levesque H1, Marie I2.[Facial diplegia as the presenting feature of Lyme disease].[Article in French] Rev Med Interne. 2015 May;36(5):352-5. doi: 10.1016/j.revmed.2014.05.002. Epub 2014 Aug 2.

148.) Elsner, R.A.; Hastey, C.J.; Olsen, K.J.; Baumgarth, N. Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. PLoS Pathog. 2015, 11, e1004976.

149.) Ramesh, G.; Didier, P.J.; England, J.D.; Santana-Gould, L.; Doyle-Meyers, L.A.; Martin, D.S.; Jacobs, M.B.; Philipp, M.T. Inflammation in the pathogenesis of Lyme neuroborreliosis. Am. J. Pathol. 2015, 185, 1344–1360.

150.) Greenberg, R. Tick-borne infections and pediatric bipolar disorder. Neurol. Psychiatry Brain Res. 2015, 22, 11.

151.) Mattingley, D.W.; Koola, M.M. Association of Lyme disease and schizoaffective disorder, bipolar type: Is it inflammation mediated? Indian J. Psychol. Med. 2015, 37, 243–246.

152.) Garakani, A.; Mitton, A.G. New-onset panic, depression with suicidal thoughts, and somatic symptoms in a patient with a history of Lyme disease. Case Rep. Psychiatry 2015, 2015.

153.) Chabria, S.; Ogbuagu, O. Fatal multiple deer tick-borne infections in an elderly patient with advanced liver disease. BMJ Case Rep. 2015.

154.) Molrine, C.J. The Experience of Lyme Disease: Cognitive-Communicative Symptomatology. In Proceedings of the Drexel University ILADS Conference, Philadelphia, PA, USA, 10 April 2015.

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:

159.) Blaut-Jurkowska J1, Jurkowski M1.[Post-Lyme disease syndrome].[Article in Polish]Pol Merkur Lekarski. 2016 Feb;40(236):129-33.

160.) Topakian R, Artemian H, Metschitzer B, Lugmayr H, Kühr T, Pischinger B. Dramatic response to a 3-week course of ceftriaxone in late neuroborreliosis mimicking atypical dementia and normal pressure hydrocephalus. J Neurol Sci. 2016 Jul 15;366:146-148. doi: 10.1016/j.jns.2016.05.002. Epub 2016 May 4.

161.) Ogrinc K1, Lusa L2, Lotric-Furlan S1, Bogovic P1, Stupica D1, Cerar T3, Ružic-Sabljic E3, Strle F1. Course and Outcome of Early European Lyme Neuroborreliosis (Bannwarth Syndrome): Clinical and Laboratory Findings. Clin Infect Dis. 2016 Aug 1;63(3):346-53. doi: 10.1093/cid/ciw299. Epub 2016 May 8

162.) Aucott, J.N.; Soloski, M.J.; Rebman, A.W.; Crowder, L.A.; Lahey, L.J.; Wagner, C.A.; Robinson, W.H.; Bechtold, K.T. CCL19 as a chemokine risk factor for posttreatment Lyme disease syndrome: A prospective clinical cohort study. Clin. Vaccine Immunol. 2016, 23, 757–766.

163.) Bransfield, R.C. Intrusive symptoms and infectious encephalopathies. Neurol. Psychiatry Brain Res. 2016, 22, 3–4.

164.) Bransfield, R.C. The assessment and treatment of sleep disorders associated with Lyme/tick-borne disease. John Drulle, MD Memorial Lecture. In Proceedings of the 17th Annual ILADS Scientific Conference, Philadelphia, PA, USA, 6 November 2016.

165.) Miklossy, J. Bacterial amyloid and DNA are important constituents of senile plaques: Further evidence of the spirochetal and biofilm nature of senile plaques. J. Alzheimers Dis. 2016, 53, 1459–1473.

166.) Waddell, L.A.; Greig, J.; Mascarenhas, M.; Harding, S.; Lindsay, R.; Ogden, N. The accuracy of diagnostic tests for Lyme disease in humans, a systematic review and meta-analysis of North American research. PLoS ONE 2016, 11, e0168613.

167.) Cook, M.J.; Puri, B.K. Commercial test kits for detection of Lyme borreliosis: A meta-analysis of test accuracy. Int. J. Gen. Med. 2016, 9, 427–440.

168.) Haney C1, Nahata MC2. Unique expression of chronic Lyme disease and Jarisch-Herxheimer reaction to doxycycline therapy in a young adult. BMJ Case Rep. 2016 Jul 20;2016. pii: bcr2013009433. doi: 10.1136/bcr-2013-009433.

169.) Víctor Ingrassia.LA NACION. 7 ABRIL 2.016. Qué es la enfermedad de Lyme, que padecen Thalía, Richard Gere y Alec Baldwin? 147.) Source:

170.) MARY BROPHY MARCUS CBS NEWS July 20, 2016, 2:19 PM. Kris Kristofferson’s Lyme disease misdiagnosed as Alzheimer’s Source:

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

173.) Branda JA1, Body BA2, Boyle J3, Branson BM4, Dattwyler RJ5, Fikrig E6, Gerald NJ7, Gomes-Solecki M8, Kintrup M9, Ledizet M10, Levin AE11, Lewinski M12, Liotta LA13, Marques A14, Mead PS15, Mongodin EF16, Pillai S17, Rao P7, Robinson WH18, Roth KM7, Schriefer ME15, Slezak T19, Snyder J20, Steere AC21, Witkowski J22, Wong SJ23, Schutzer SE24. Advances in Serodiagnostic Testing for Lyme Disease Are at Hand. Clin Infect Dis. 2017 Dec 7. doi: 10.1093/cid/cix943. [Epub ahead of print]

174.) Gordillo-Pérez G1, García-Juárez I1, Solórzano-Santos F2, Corrales-Zúñiga L3, Muñoz-Hernández O2, Torres-López J1. Serological Evidence of Borrelia Burgdorferi Infection in Mexican Patients with Facial Palsy. Rev Invest Clin. 2017 Nov-Dec;69(6):344-348. doi: 10.24875/RIC.17002344.

175.) Greenberg, R. Infections and childhood psychiatric disorders: Tick-borne illness and bipolar disorder in youth. Bipolar Disord. 2017, 3, 113.

176.) Bransfield, R.C. Suicide and Lyme and associated diseases. Neuropsychiatr. Dis. Treat. 2017, 13, 1575–1587.

177.) Luché-Thayer, J.; Ahern, H.; DellaSala, D.; Franklin, S.; Gilbert, L.; Horowitz, R.; Liegner, K.; McManus, M.; Meseko, C.; Miklossy, J.; et al. Updating ICD11 Borreliosis Diagnostic Codes: Edition One; CreateSpace Independent Publishing Platform: North Charleston, NC, USA, 2017; ISBN-10 1978091796; ISBN-13 978-1978091795.

178.) Alonso, L.; Raymond, P. Complex chronic infections in autistic children. In Proceedings of the ILADS 2017 European Conference, Paris, France, 19 May 2017.

179.) Kucharska, M. Child with autism, mother with Lyme—Congenital Borreliosis? In Proceedings of the 18th Annual ILADS Scientific Conference, Boston, MA, USA, 9–12 November 2017.

180.) Rebman, A.W.; Bechtold, K.T.; Yang, T.; Mihm, E.A.; Soloski, M.J.; Novak, C.B.; Aucott, J.N. The clinical, symptom, and quality-of-life characterization of a well-defined group of patients with posttreatment Lyme disease syndrome. Front. Med. (Lausanne) 2017, 4, 224.

181.) Oczko-Grzesik, B.; Kepa, L.; Puszcz-Matlinska, M.; Pudlo, R.; Zurek, A.; Badura-Glabik, T. Estimation of cognitive and affective disorders occurrence in patients with Lyme borreliosis. Ann. Agric. Environ. Med. 2017, 24, 33–38.

182.) Patient Registry, MyLymeData, Phase 1. 27 April 2017. Available online: (accessed on 30 August 2018).

183.) Hanna, A.F.; Abraham, B.; Hanna, A.; Smith, A.J. Effects of intravenous ketamine in a patient with post-treatment Lyme disease syndrome. Int. Med. Case Rep. J. 2017, 10, 305–308.

184.) Blum, K.; Modestino, E.J.; Febo, M.; Steinberg, B.; McLaughlin, T.; Fried, L.; Baron, D.; Siwicki, D.; Badgaiyan, R.D. Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission. J. Syst. Integr. Neurosci. 2017, 3.

185.) Staff. In NY Follow-up Letter, Dr. Bransfield Connects Lyme to Opioid Crisis., 6 September 2017. Available online:–sleeper&utm_campaign=sept+5–sleeper+cells&utm_medium=email (accessed on 30 august 2018).

186.) Pisa, D.; Alonso, R.; Fernández-Fernández, A.M.; Rábano, A.; Carrasco, L. Polymicrobial infections in brain tissue from Alzheimer’s disease patients. Sci. Rep. 2017, 7, 5559.

187.) Beridze M1, Khizanishvili N1, Mdivani M1, Samushia O1, Gogokhia N1. UNUSUAL MANIFESTATION OF NEUROBORELIOSIS (CASE REPORT). Georgian Med News. 2017 Mar;(264):72-75.

188). CLAUDIA TANNER FOR MAILONLINE PUBLISHED: 16:10 BST, 18 September 2017 | UPDATED: 16:55 BST, 18 September 2017. Yolanda Hadid says her Lyme disease was misdiagnosed as ME … Source:

189.) Alec Baldwin latest celebrity to battle Lyme disease: What is it? source:  MAY 23 / 2017

190.) Lapenta J., Lapenta JM. UNDERSTANDING THE LYME DISEASE, CLASSIFICATION AND CODES. Investigative Dermatology and Venereology Research. Publish Date : 2018-01-12 source:,-CLASSIFICATION-AND-CODES./1769



193.) Kristoferitsch W, Aboulenein-Djamshidian F, Jecel J, Rauschka H, Rainer M, Stanek G, Fischer P. Secondary dementia due to Lyme neuroborreliosis. Wien Klin Wochenschr. 2018 Jul 25. doi: 10.1007/s00508-018-1361-9. [Epub ahead of print]

194.) Koster MP1, Garro A2. Unraveling Diagnostic Uncertainty Surrounding Lyme Disease in Children with Neuropsychiatric Illness. Child Adolesc Psychiatr Clin N Am. 2018 Jan;27(1):27-36. doi: 10.1016/j.chc.2017.08.010. Epub 2017 Oct 21.

195.) Faber, S. 32 Years of Documentation of Maternal-Child Transmission of Lyme Disease and Congenital Lyme Borreliosis 2018. Available online: (accessed on 28 august 2018).

196.) Johnco, C.; Kugler, B.B.; Murphy, T.K.; Storch, E.A. Obsessive-compulsive symptoms in adults with Lyme disease. Gen. Hosp. Psychiatry 2018, 51, 85–89.

197.) Weinstein, E.R.; Rebman, A.W.; Aucott, J.N.; Johnson-Greene, D.; Bechtold, K.T. Sleep quality in well-defined Lyme disease: A clinical cohort study in Maryland. Sleep 2018, 41.

198.) Liu, S.; Cruz, I.D.; Ramos, C.C.; Taleon, P.; Ramasamy, R.; Shah, J. Pilot study of immunoblots with recombinant Borrelia burgdorferi antigens for laboratory diagnosis of Lyme disease. Healthcare 2018, 6, 99.

199.) Doshi, S.; Keilp, J.G.; Strobino, B.; McElhiney, M.; Rabkin, J.; Fallon, B.A. Depressive symptoms and suicidal ideation among symptomatic patients with a history of Lyme diseaHealthcare 2018, 6(3), 104; doi:10.3390/healthcare6030104

200.) Staff. How Many People Ger Lyme Disease? CDC. Available online: (accessed on 10 august 2018).

201.) Faber, S. 32 Years of Documentation of Maternal-Child Transmission of Lyme Disease and Congenital Lyme Borreliosis 2018. Available online: (accessed on 20 august 2018).

202.) Greenberg, R. Aggressiveness, violence, homicidality, homicide, and Lyme disease. Letter to the editor. Neuropsychiatr. Dis. Treat. 2018, 14, 1253–1254

203.) Robert C. Bransfield. Neuropsychiatric Lyme Borreliosis: An Overview with a Focus on a Specialty Psychiatrist’s Clinical Practice. Open Access Healthcare 2018, 6(3), 104; doi:10.3390/healthcare6030104

204.) Helen Fosam, PhD. RHEUMATOLOGY ADVISOR. Diagnosing Lyme Disease in Children With Neuropsychiatric Illness. Helen Fosam, PhD. July 27, 2018, Source:

205.) Koster MP1, Garro A2. Unraveling Diagnostic Uncertainty Surrounding Lyme Disease in Children with Neuropsychiatric Illness. Child Adolesc Psychiatr Clin N Am. 2018 Jan;27(1):27-36. doi: 10.1016/j.chc.2017.08.010. Epub 2017 Oct 21.

206.) LYme After A 5 Year Break, Avril Lavigne to Drop a New Album About Her Battle with Lyme Disease. Source:


208.) PRESS RELEASE: Ground Breaking Recognition of Lyme Borreliosis in 11th International Classification of Diseases. Source:



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