lunes, 31 de diciembre de 2018



The Post-Lyme Disease Treatment Syndrome (PTLDS) a review of its origin and its consequences in the socio-economic sphere.
Lapenta J1*, Lapenta JM2

1Lapenta, J.  Medic Surgeon, Specialty Dermatology. Member of the Ad Hoc committee for the Lyme disease codes ICD-11 as an expert reviewer, University of Carabobo, Venezuela. Ceo Dermagic Express.
2Lapenta, J.M. Medic Surgeon. University of Carabobo. Diplomat in  Body and Facial Aesthetics, Occupational Medicine, Prehospital Auxiliary, and Integral Ultrasound.  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:


In the 90s began to describe a set of signs and symptoms in patients who after being diagnosed with Lyme disease, which is caused by the bite of a tick, which transmits the spirochete Borrelia Burgdorferi, living agent that causes all this symptomatology. These symptoms that were described months after having concluded the treatment of the disease began to be reported by various scientists around the world and were called Post Treatment Lyme Disease Syndrome (PTLDS), mainly characterized by cognitive deterioration, recurring headaches, fatigue, memory problems, musculoskeletal pain and many others. For some organizations the syndrome is true, for others it is only a psychosomatic disease squeal of Lyme disease, leaving out of treatment the thousands of people who present these symptoms after treatment of Lyme today; there is now a great controversy surrounding this issue. In this research we will make a chronological description of this post-Lyme syndrome, when it appeared, its symptoms and if it really deserves to be recognized by the World Health Organization (WHO) in the new ICD-11 codes whose deadline for it is May of 2,019. In addition to this aspect, clarify the true meaning of this term and scope in medical and non medical society; also propose a treatment for this disease that could eliminate this bacterium that is causing so much deterioration in the affected population worldwide.


• Make a chronological description of the post treatment Lyme disease syndrome (PTLDS) from its beginnings to the present, its clinical characteristics in all affected age groups regardless of sex, age, race and nations.


• Determine if this Post Lyme Syndrome is a scientific reality that should be:
• Considered within the new ICD-11 codes (International Classification of Diseases year 2.018). ?
• It is a sequential psychosomatic disease after the treatment of Lyme disease. ?
• It really exists as a clinical entity but its term or definition is poorly implemented. ?
• Propose a new alternative treatment for Lyme disease that would mainly cover the second, third and sequel of the same, a topic that we are considering in the present investigation.


The methods to be used are fundamentally based on making an analysis of all the databases and articles published in this regard, both for or against Lyme disease post treatment syndrome (PTLDS), fundamentally the National Library of Medicine of the USA. (Pubmed, Medline). Scientific and technical literature on Health in Latin America and the Caribbean (LILACS), and Europe (SCOPUS, EMBASE); make a chronological description of the post-treatment syndrome of Lyme disease from the first time it was mentioned in the scientific literature to the present day, highlighting the most relevant. Consider based on the findings found the objectives we set, determine if this syndrome is a reality, is a psychosomatic disease or its definition is poorly structured, describing the term given to this syndrome by the CDC (Center for the control and prevention of Diseases) and the one described by the scientists in their investigations. In addition to that, we will explain why this term is causing so much controversy today, before few months of the recognition of the new ICD-11 codes for Lyme disease; and finally we will propose a new treatment that should be considered by the world health authorities for the treatment of this disease.

In the chronology of post-treatment Lyme disease syndrome (PTLDS) we will highlight the most relevant ones in the timeline, describing the term first, by the health authorities (CDC) and by the scientists concerned to study these clinical manifestations.



The CDC says textually: “Lyme disease is an infection caused by the bacterium Borrelia burgdorferi. In the majority of cases, it is successfully treated with oral antibiotics. Physicians sometimes describe patients who have non-specific symptoms (like fatigue, pain, and joint and muscle aches) after the treatment of Lyme disease as having post-treatment Lyme disease syndrome (PTLDS) or post Lyme disease syndrome (PLDS). The cause of PTLDS is not known.”

The CDC also dismisses the use of the term "Chronic Lyme Disease" (CLD), arguing that this term is confusing in the scientific community and has been used at times to describe symptoms in patients who "never had actual or past contact" with Borrelia Burgdorferi infection. [1]

In summary: for the CDC, one of the entities perhaps the most important in the USA, this Post-treatment of Lyme disease syndrome (PTLDS) is of "unknown cause" and in addition he alleges that the term "Chronic Lyme Disease" (CLD) should not be used, it does not exist, because most patients are "cured" with adequate antibiotic therapy.


Lyme disease is caused by a bacterium Borrelia Burgorferi. Many patients, months or years after being properly diagnosed and treated with antibiotic therapy, show persistent neurological and organic symptoms (post-treatment Lyme disease syndrome (PTLDS), among which the following stand out: cognitive alterations: memory loss, verbal flexibility, association, speed of thought, fatigue, musculoskeletal pain, weakness and many others, being the cause of this a chronic encephalopathy caused by the Borrelia burgdorferi when reach brain, because this bacterium as Treponema pallidum (syphilis) is highly neurotropic what it means that it has an affinity for nerves and brain tissue. [2]
Also many, perhaps most researchers recognize the term "Chronic Lyme Disease (CLD), widely described in the literature [2], and that would be the same post-treatment Lyme disease syndrome (PTLDS). In addition, they consider that in many cases the diagnosis was made late due to failures in the blood tests and resistance to the treatment with antibiotics.
In summary: for the scientific community, the term "post-treatment of Lyme disease syndrome (PTLDS)" is a reality and, in many cases, the cause of this is a chronic encephalopathy that causes the symptoms. The failure of the treatment with antibiotics, or the late establishment of it by missdiagnoses, could contribute in all that symptomatology; therefore, there was no "success in healing", which contradicts what was stated by the CDC.



In the year 1.991 Krupp, L.B, et al. [3], 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; memory deterioration did not correlate with anti-Borrelia burgoderferi antibodies in blood or cerebrospinal fluid, nor was evidence found in magnetic resonances made to affected patients or to symptoms of depression. The authors conclude that it is an encephalopathy of unknown cause, where factors such as the sequel of systemic infection by Borrelia and other toxic metabolic factors may be partly responsible for these symptoms.

Perhaps this represents the first study, 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. [3]

Note: In all the previous studies of Lyme Neuroborreliosis this term is not mentioned, it is spoken of the chronic manifestations of the disease as part of the second or late phase of the same, but not with the term "post-treatment" until 1.991 where these researchers publish this study. [2-3]


After the description of Krupp et al., another scientists Benke, T. et al. [4], in the year of 1995, published a study on 20 patients with Lyme Borreliosis previously diagnosed several years earlier, with an average of 4.3 years after the acute phase of Lyme, compared with a control group; This study revealed that patients with Lyme revealed deficits in verbal memory, mental flexibility, verbal associative functions and vocal articulation. The authors suggest that these findings are similar to those reported by Krupp et al. in 1991 and reaffirm that it is an encephalopathy associated with a long-term neuropsychological deficit that predominantly affects internal functions. [4]


One year later Bujak, DI. Et al. in 1.996  published a study of 23 patients of 23 years of age after had Lyme positively tested with ELISA, and previously treated with standard antibiotic regimens for the disease; Neurocognitive impairment, persistent arthralgia, fatigue and memory loss were evaluated, finding the following facts: 7 patients (30%) had fibromyalgia, 3 (13%) had chronic fatigue syndrome and 22 of 23 (almost 100%), they complained about memory problems or decreased concentration. The scores for the attention scale, verbal memory, visual memory, sleep problems, mood swings and depression symptoms were higher for Post Lyme patients (PLS) than the normal scales.

The authors conclude that despite treatment with appropriate antibiotics for Lyme disease may be sequels, mainly neurocognitive disorders, persistent arthralgias and fatigue. [5]


In this year, Gaudino, E.A. et al. published a study to evaluate the differences and similarities between chronic fatigue syndrome (CFS) and post-Lyme syndrome (PLS) studying 25 patients with chronic fatigue syndrome (CFS) with exclusion criteria for Lyme disease, 56 healthy controls and 38 patients with Post Lyme syndrome (PLS), seropositive for Borrelia burgdorferi with positive criteria by the CDC for Lyme, who presented symptoms of severe fatigue 6 months after having complied with the treatment of antibiotics for Lyme disease. All the patients underwent structured psychiatric interviews, evaluating: attention tests, verbal memory, verbal fluency and motor speed.

Patients with chronic fatigue syndrome (CFS) and Post Lyme syndrome (PLS) were similar in several somatic symptoms and in the psychiatric profile. Patients with PLS had a worse performance on cognitive tests compared to healthy controls.

The authors conclude that despite the overlap of symptoms, patients with Post Lyme Syndrome (PLS) show greater cognitive deficits than patients with Chronic Fatigue Syndrome (CFS) compared to healthy controls. This fact became more evident among patients with PLS who lacked premorbid psychiatric disease. [6]


Bloom, BJ et al. in 1998 they studied 5 children from the neurocognitive point of view after having been diagnosed with Lyme disease being seropositive for Borrelia burgdorferi, finding intrathecal antibodies against the spirochete. They were treated for 2 to 4 weeks with intravenous ceftriaxone and evaluated comprehensively including detailed neuropsychiatric tests. The main objective of the study was to consider the possibility that Lyme disease after treatment left a sequel in children as well, as it had already been demonstrated in adults.

The 5 children were followed up for a period of 2 to 7 years after the treatment with antibiotic (ceftriaxone) and it was found that months after the treatment the children after having had the classic erythema migrans, cranial neuropathy or Lyme arthritis, developed behavioral changes, forgetfulness, decreased school performance, headache, fatigue and in two cases complex seizure disorders.

The five patients were found IgG antibodies against Borrelia burgdorferi in serum, intrathecal IgG antibodies and two of them pleocytosis of the cerebrospinal fluid (CSF). Despite normal intellectual functioning, the five children had mild to moderate impairments in auditory or visual sequential processing.

The authors conclude that children can develop neurocognitive symptoms together with or after the classic manifestations of Lyme disease, and attribute it to an infectious or postinfectious encephalopathy related to Borrelia Burgdorferi, confirming previous studies in adults [7], [3], [4].

In this study it was demonstrated that the post-treatment syndrome of Lyme disease (PTLDS) not only affects adults, but also children can be affected, and it is reaffirmed that the cause of it is an encephalopathy caused by the infection of the Borrelia burgdorferi.


In the year of 1.999 Elkins LE, et al. published a work on 30 patients with Post Lyme Syndrome (PLS), who were surveyed to determine the neuropsychological status found as a fundamental aspect that: the mood of PLS ​​participants was characterized by reduced levels of positive affect (PA) and typical levels of negative affect, concluding that the authors that these symptoms are the most useful markers in patients with Post Lyme Syndrome (PLS). [8]

That same year of 1,999 Kaplan RF, et al. conducted a study where they claim that a small group of patients with Lyme develop encephalopathic symptoms mild to moderate months to years after diagnosis and treatment. The most common symptoms reported are fatigue, memory loss, sleep disorders and depression with a controversial etiology of the syndrome (PLS). The study was done comparing patients with Lyme and abnormal cerebrospinal fluid (CSF), patients with Lyme and normal CSF and healthy controls. Both groups with Lyme showed memory deficits, but more accentuated and measurable in those with abnormal CSF; they also showed higher score in the depression aspect in relation to healthy controls. [9]


In the year 2001 Klemper MS, et al. conducted a study to test the efficacy of antibiotic treatment in Lyme-positive patients with persistent symptoms and a history of Lyme disease. Two groups of patients were studied: 78 seropositive patients and 51 seronegative patients for Borrelia Burgdorferi. Patients received intravenous ceftriaxone, 2 g daily for 30 days, followed by oral doxycycline, 200 mg daily for 60 days, or corresponding oral and intravenous placebos. Each patient had well documented and treated Lyme disease, and had persistent musculoskeletal pain, or dysesthesia associated with fatigue. 

The authors conclude that there is a considerable deterioration in health-related quality of life among patients with persistent symptoms despite prior treatment for acute Lyme disease. In these two trials treatment with oral or intravenous antibiotics for 90 days did not improve symptoms more than placebo. [10]

This year of 2.001 Morgen K, et al. performed a brain magnetic resonance (MR) study in 27 patients with post-treatment Lyme disease syndrome to try to help identify the pathological mechanisms of the disease. Of the total, four (4) patients had focal neurological deficits, recurrent remitting disease and lesions in a typical electron microscopy (EM) distribution; 23 (85%) patients presented non-focal symptoms, such as fatigue, subjective memory deficiencies and mood disorders. Twelve of these patients (44%) had normal magnetic resonance imaging (MRI); 10 (37%) had mainly punctate and subcortical lesions, and one patient had multiple periventricular lesions.

The authors conclude that in a portion of patients with Lyme disease syndrome after treatment, hyperintensities of the white matter tend to occur in subcortical arteriolar watershed areas and are not specific. [11]

These last two studies show conclusively two facts: 1.) Many patients DO NOT IMPROVE with long-term antibiotics after presenting chronic symptoms post Lyme and 2.) It is demonstrated that there are obvious findings of the damage of the cerebral white matter in post-Lyme patients treatment, found by means of magnetic resonance imaging (MRI).

This means that in the line of time and for the 90s and the beginning of the 2000s, a harsh reality is uncovered: Lyme disease is an illness that in many cases becomes chronic, months or years after having started his symptoms, even after having disappeared also after proper treatment.

To not make it longer we will place you the most frequent symptoms found and described by other qualified scientists in the almost last 20 years about Chronic Lyme Disease (CLD) or post-treatment Lyme disease syndrome (PTLDS):



1.) Fatigue and lack of resistance,
2.) Nocturnal sweating.
3.) Pale, dark circle under the eyes.
4.) Abdominal pain.
5.) Diarrhea or constipation.
6.) Nausea.
7.) Cardiac anomalies: Lyme carditis 
8.) Orthopedic disorders: sensitivity, spasms and generalized muscle pain, rigidity and / or retarded motion.
9.) Respiratory infections of the superior tract and otitis.
10.) Arthritic disorders and painful joints.
11.) Neurological disorders:

      A.) Headache.
      B.) Drowsiness.
      C.) Loss of memory.
      D.) Convulsions.
      E.)  Facial paralysis
      F.) Irritability.
      G.) Bad mood.

12.) Suicidal thoughts.
13.) Anxiety.
14.) Anger or rage
15.) Hallutinations.
16.) Earning disorders and humor changes:

       A-) Cognitive speaking.
       B-) Speech delay.
       C-) Reading-writing problems.
       D.) Problems of vocal articulation.
       E-) Auditory / visual processing problems.
       F-) Word selection problems.
       G-) Dyslexia.

17.) Aggression or violence.
18.) Irritability,
19.) Emotional disorders.
20.) Depression.
21.) Hyperactivity.
22.) Photophobia.
23.) Gastroesophageal reflux with vomiting and coughing.
24.) Secondary eruptions.
25.) Other eruptions.
26.) Ocular problems: posterior cataracts, myopia, stigmatism, conjunctive erythema 
(Lyme eyes), optical nerve atrophy and / or uveitis.
27.) Sensitivity of skin and noise (hyperacuity).
28.) Demyelinization of the nervous system.[12-45]

Probably there are more, the evidence is that there really are chronic symptoms in Lyme disease, with or without adequate treatment. For no one is a secret of the large number of patients in North America, Europe and Asia who suffer from chronic Lyme. The bibliographical references presented in this research and the others that we have published are too strong. [2-45]


1.) It is demonstrated that the chronic symptoms of Lyme disease are a reality  both in adults and childrens; some scientists call it:

A.) Chronic Lyme disease (CLD); others:
B.) Syndrome- Post-treatment of Lyme disease (PTLDS).

As we said at the beginning, the CDC does not recognize the term Chronic Lyme Disease (CLD) because it is confusing and alleges that the majority of patients are cured after an adequate treatment with antibiotics. [1]

• With respect to this, we conclude that the CDC is totally wrong because it is demonstrated that months or years after adequate treatments with antibiotics, the patients have the same or worse symptoms, which gives truth to the term: chronic Lyme disease (CLD), which they deny themselves.

On the other hand, the CDC alleges that the term Post-treatment of Lyme disease syndrome  (PTLDS) is used by some scientists to define symptoms after the treatment of the disease and that it is due to “unknown cause”:

• With regard to this aspect, the "so called” Post-treatment of Lyme disease syndrome (PTLDS), is the same chronic Lyme disease, consisting of:

A.) Lyme positive patients who were never treated.

B.) Positive Lyme patients who after treatment in acute phase relapsed months or years later, and reached the secondary or late stage with symptoms equal or more severe than at the beginning.

C.) Patients who were misdiagnosed due to lack of effective diagnostic tests and reached the chronic stage. Today the CDC recognizes that its diagnostic tests are not 100% effective.

D.) Well-diagnosed Lyme patients who never responded to the treatments recommended by the CDC.

• We also conclude that the CDC is wrong about the definition of "unknown cause" when most studies and research show that it is a chronic encephalopathy produced by Borrelia Burgdorferi, Either by:

• Its persistence in the bloodstream, cerebrospinal fluid and tissues due to resistance to treatment, under the well-known mechanism of "Biofilm".

• For the generation of neurological damage due to the persistence of Borrelia Burgdorferi in tissues that do not regenerate, such as the nerve cells.

• Or inflammatory processes that remained chronically in the nervous system and tissues after eliminating the causative agent, which is debatable today.

 2.) The coexistence of other diseases such as Erlichiosis, Babesiosis and Bartonella, which at the end, what they do is worsen the symptoms and hinder the treatment.

3.) We find with an unprotected society, the reality is that thousands of patients are discarded as positive Lyme after 4 months of treatment, because the treatment guidelines of the CDC say that in that time or less you will be cured, which we prove is false in a good proportion of patients.

4.) In May is the limit for the recognition of ICD-11 CODES (International classification of diseases, year 2.018) for Lyme disease and some countries refuse to recognize them all, which would make the affected society even worse, I mean the code: Congenital Lyme. [46-51]

5.) The global community of patients with Lyme must organize well and adequately claim from health authorities such as the World Health Organization (WHO) to recognize the entire Lyme codes, and ensure coverage of their treatment in all levels.

6.) The Syndrome post-treatment of Lyme disease (PTLDS), which is nothing more than the ”chronic symptoms” of the disease, is being used perversely to cover the reality of this disease, avoid coverage by health insurance, and tell the patients: "you have nothing, go to a psychologist ... when your blood and brain are sailing in a sea of ​​Borrelias.

Dr. José Lapenta Dermatologist
Dr. José M. Lapenta Md.


To the Lyme world community that fights for its rights to be treated as real patients and not as psychiatric patients.

To my son J. Miguel MD, for his logistical support and co-author.

To all patients with Lyme especially Stacy Cellier Gomez whose story was quite motivating.


1.) CDC. Centers for Disease Control and Prevention. Post-Treatment Lyme Disease Syndrome. (2018) revised November 21, 2018. Source:

2.){Lapenta J, Lapenta J.M,. Lyme Disease and Dementia, Alzheimer, Parkinson, Autism, an Easy Way to Destroy your Brain},Investigative Dermatology and  Venereology Research},2018. 4(1):30-43} (Ommega publishers),,-Alzheimer,-Parkinson,-Autism,-an-easy-way-to-destroy-your-brain./1992

3.) 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.

4.) Benke, T., Gasse, T., Hittmair-Delazer, M., et al. Lyme encepha- lopathy: Long-term neuropsychological deficits years after acute neuroborreliosis. (1995) Acta Neurol. Scand 91(5): 353-357. Pubmed| Crossref| Others

5.) Bujak DI, Weinstein A, Dornbush RL. Clinical and neurocognitive features of the post Lyme syndrome. J Rheumatol. 1996 Aug;23(8):1392-7.

6.) Gaudino, E.A., Coyle, P.K., Krupp, L.B. Post-Lyme syndrome and chronic fatigue syndrome. Neuropsychiatric similarities and dif- ferences. (1997 ) Arch Neurol 54(11): 1372

7.) Bloom BJ1, Wyckoff PM, Meissner HC, Steere AC. Neurocognitive abnormalities in children after classic manifestations of Lyme disease. Pediatr Infect Dis J. 1998 Mar;17(3):189-96.

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

9.) 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. 

10.) Klempner MS1, Hu LT, Evans J, Schmid CH, Johnson GM, Trevino RP, Norton D, Levy L, Wall D, McCall J, Kosinski M, Weinstein A.Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med. 2001 Jul 12;345(2):85-92.

11.) Morgen K1, Martin R, Stone RD, Grafman J, Kadom N, McFarland HF, Marques A.. FLAIR and magnetization transfer imaging of patients with post-treatment Lyme disease syndrome. Neurology. 2001 Dec 11;57(11):1980-5.

9.) Weinstein A1, Britchkov M. Lyme arthritis and post-Lyme disease syndrome.Curr Opin Rheumatol. 2002 Jul;14(4):383-7.

10.) Shotland LI1, Mastrioanni MA, Choo DL, Szymko-Bennett YM, Dally LG, Pikus AT, Sledjeski K, Marques A.Audiologic manifestations of patients with post-treatment Lyme disease syndrome. Ear Hear. 2003 Dec;24(6):508-17.

11.) Steven E Phillips  Joseph J Burrascano  Nick S Harris  Lorraine Johnson  Patricia V Smith Raphael B Stricker. Chronic infection in ‘post-Lyme borreliosis syndrome’ .International Journal of Epidemiology, Volume 34, Issue 6, 1 December 2005, Pages 1439–1440,

12.) Cairns V1, Godwin J. Post-Lyme borreliosis syndrome: a meta-analysis of reported symptoms.Int J Epidemiol. 2005 Dec;34(6):1340-5. Epub 2005 Jul 22.

13.) Pícha D, Moravcova L, Lasikova S, Holeckova D, Maresova V. Symptoms of post-Lyme syndrome in long-term outcome of patients with neuroborreliosis. Scand J Infect Dis. 2006;38(8):747-8.

14.) Pfister HW1, Rupprecht TA. Clinical aspects of neuroborreliosis and post-Lyme disease syndrome in adult patients. Int J Med Microbiol. 2006 May;296 Suppl 40:11-6. Epub 2006 Mar 9.

15.) Auwaerter PG1. Point: antibiotic therapy is not the answer for patients with persisting symptoms attributable to lyme disease. Clin Infect Dis. 2007 Jul 15;45(2):143-8. Epub 2007 Jun 5.

16.) Stricker RB1. Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with lyme disease. Clin Infect Dis. 2007 Jul 15;45(2):149-57. Epub 2007 Jun 5.

17.) McAuliffe P1, Brassard MR, Fallon B. Memory and executive functions in adolescents with posttreatment Lyme disease. Appl Neuropsychol. 2008;15(3):208-19. doi: 10.1080/09084280802324473.

18.) Hassett AL1, Radvanski DC, Buyske S, Savage SV, Gara M, Escobar JI, Sigal LH. Role of psychiatric comorbidity in chronic Lyme disease. Arthritis Rheum. 2008 Dec 15;59(12):1742-9. doi: 10.1002/art.24314.

19.) Moniuszko A1, Czupryna P, Zajkowska J, Pancewicz SA, Grygorczuk S, Kondrusik M. Pol Merkur Lekarski [Post Lyme syndrome as a clinical problem]. 2009 Mar;26(153):227-30. [Article in Polish]Pol Merkur Lekarski. 2009 Mar;26(153):227-30.

20.) Moniuszko A1, Czupryna P, Zajkowska J, Pancewicz SA, Grygorczuk S, Kondrusik M. [Post Lyme syndrome as a clinical problem]. Pol Merkur Lekarski. 2009 Mar;26(153):227-30.[Article in Polish]

21.) Clarissou J1, Song A, Bernede C, Guillemot D, Dinh A, Ader F, Perronne C, Salomon J., Efficacy of a long-term antibiotic treatment in patients with a chronic Tick Associated Poly-organic Syndrome (TAPOS). Med Mal Infect. 2009 Feb;39(2):108-15. doi: 10.1016/j.medmal.2008.11.012. Epub 2009 Jan 4.

21.) Markeljevic J1, Sarac H, Rados M.Tremor, seizures and psychosis as presenting symptoms in a patient with chronic lyme neuroborreliosis (LNB).Coll Antropol. 2011 Jan;35 Suppl 1:313-8.

22.) Schutzer SE1, Angel TE, Liu T, Schepmoes AA, Clauss TR, Adkins JN, Camp DG, Holland BK, Bergquist J, Coyle PK, Smith RD, Fallon BA, Natelson BH. Distinct cerebrospinal fluid proteomes differentiate post-treatment lyme disease from chronic fatigue syndrome. PLoS One. 2011 Feb 23;6(2):e17287. doi: 10.1371/journal.pone.0017287.

23.) Chandra A1, Wormser GP, Marques AR, Latov N, Alaedini A. Anti-Borrelia burgdorferi antibody profile in post-Lyme disease syndrome. Clin Vaccine Immunol. 2011 May;18(5):767-71. doi: 10.1128/CVI.00002-11. Epub 2011 Mar 16.

24.) Fallon BA1, Petkova E, Keilp JG, Britton CB. A reappraisal of the u.s. Clinical trials of post-treatment lyme disease syndrome.
Open Neurol J. 2012;6:79-87. doi: 10.2174/1874205X01206010079. Epub 2012 Oct 5.

25.) 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.

26.) Aucott JN1, Rebman AW, Crowder LA, Kortte KB. Post-treatment Lyme disease syndrome symptomatology and the impact on life functioning: is there something here? Qual Life Res. 2013 Feb;22(1):75-84.

27.) Aucott JN1, Crowder LA, Kortte KB. Development of a foundation for a case definition of post-treatment Lyme disease syndrome. Int J Infect Dis. 2013 Jun;17(6):e443-9. doi: 10.1016/j.ijid.2013.01.008. Epub 2013 Feb 23.

28.) Batheja S, Nields JA, Landa A, Fallon BA. Post-treatment lyme syndrome and central sensitization. J Neuropsychiatry Clin Neurosci. 2013 Summer;25(3):176-86. doi: 10.1176/appi.neuropsych.12090223.

29.) Crowder LA1, Yedlin VA2, Weinstein ER3, Kortte KB4, Aucott JN5. Lyme disease and post-treatment Lyme disease syndrome: the neglected disease in our own backyard. Public Health. 2014 Sep;128(9):784-91. doi: 10.1016/j.puhe.2014.06.016. Epub 2014 Sep 9.

30.) 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.

31.) Weitzner E1, McKenna D1, Nowakowski J1, Scavarda C1, Dornbush R2, Bittker S1, Cooper D1, Nadelman RB1, Visintainer P3, Schwartz I4, Wormser GP1. Long-term Assessment of Post-Treatment Symptoms in Patients With Culture-Confirmed Early Lyme Disease. Clin Infect Dis. 2015 Dec 15;61(12):1800-6. doi: 10.1093/cid/civ735. Epub 2015 Sep 18.

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

33.) Nemeth J1, Bernasconi E2, Heininger U3, Abbas M4, Nadal D5, Strahm C6, Erb S7, Zimmerli S8, Furrer H8, Delaloye J9, Kuntzer T10, Altpeter E11, Sturzenegger M12, Weber R1, For The Swiss Society For Infectious Diseases And The Swiss Society For Neurology. Update of the Swiss guidelines on post-treatment Lyme disease syndrome. Swiss Med Wkly. 2016 Dec 5;146:w14353. doi: 10.4414/smw.2016.14353. eCollection 2016.

34.) 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.

35.) Rebman AW1,2, Aucott JN2, Weinstein ER1,2, Bechtold KT2, Smith KC3, Leonard L3,4. Living in Limbo: Contested Narratives of Patients With Chronic Symptoms Following Lyme Disease. Qual Health Res. 2017 Mar;27(4):534-546. doi: 10.1177/1049732315619380. Epub 2016 Jul 10.

36.) 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. 

37.) 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. 

38.) Weinstein ER1, Rebman AW1, Aucott JN1, Johnson-Greene D2, Bechtold KT3,4. Sleep quality in well-defined Lyme disease: a clinical cohort study in Maryland. Sleep. 2018 May 1;41(5). doi: 10.1093/sleep/zsy035.

39.) Cervantes J1. Doctor says you are cured, but you still feel the pain. Borrelia DNA persistence in Lyme disease. 
Microbes Infect. 2017 Sep - Oct;19(9-10):459-463. doi: 10.1016/j.micinf.2017.06.002. Epub 2017 Jun 15.

40.) Touradji P1, Aucott JN2, Yang T2, Rebman AW2, Bechtold KT1. Cognitive Decline in Post-treatment Lyme Disease Syndrome. Arch Clin Neuropsychol. 2018 Jun 26. doi: 10.1093/arclin/acy051. [Epub ahead of print]

41.) Davidsson M1. Healthcare (Basel). 2018 Feb 13;6(1). pii: E16. doi: 10.3390/healthcare6010016.
The Financial Implications of a Well-Hidden and Ignored Chronic Lyme Disease Pandemic.

42.) Lapenta, J. Lapenta J.M., Lyme disease and dementia, Alzheimer, Parkinson, Autism, an easy way to destroy your brain. Investigative Dermatology and Venereology Research. Source:

43.) Lapenta J, Lapenta JM. understanding the Lyme disease, Classificationm and codes. Ommega Publisher (2.018) Source:,-CLASSIFICATION-AND-CODES./1769



46.)  Centers for Disease Control, USA. yme Disease. Data and Statistics (Consultado 2.018, 19 junio) disponible en:

47.) Online ICD9/ICD9CM codes. Source:

48.) ICD-10 Version 2.016. Source:

49.) 2018 New ICD-10-CM Codes. Source:

50.) Information from World Health Organization (WHO): List of Official ICD-10 Updates. For the ICD-11 revision: The ICD 11th Revision is due by 2017 (Archived, Feb. 2014); ICD Revision Timelines and ICD-11 Beta Draft (online beta-version of ICD-11). Source:

51.) International Statistical Classification of Diseases and Related Health Problems. Source:



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