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Lyme Disease has Effects on the Brain

IT IS IN THE HUMAN BRAIN IN HOURS TO UNDER TEN DAYS

IF SYPHILIS CAUSES MASSIVE BRAIN DAMAGE AND LYME IS MUCH STRONGER WHY WASTE TIME DEBATING THIS ISSUE?

IF REIK, IN HIS TEXTBOOK, LYME AND THE CENTRAL NERVOUS SYSTEM, 1991, SHOWS MASSIVE BRAIN DAMAGE BY LYME WHY CANNOT SMALLER MERE BIOCHEMICAL DAMAGE AND INFLAMMATION CAUSE PSYCHIATRIC TROUBLES?

1. Neuroborreliosis: a psychiatric problem?

Article in Polish

Popławska R, Szulc A, Zajkowska J, Pancewicz S.

Source

The authors review the literature concerning clinical characteristics of neuroborreliosis with special focus on mental disorders. The patients develop mental disorders during the acute phase of the disease and even after several years. These disorders are often accompanied with various neurological syndromes. The authors discuss the most common mental disorders connected with neuroborreliosis: encephalopathy, cognitive disorders, dementia, depression, anxiety disorders. The paper describes the problem of neuroborreliosis in psychiatry, especially in the endemic regions. Neurobiol Dis. 2010 Mar;37(3):534-41. Epub 2009 Nov 26.

Inflammation and central nervous system Lyme disease.

Fallon BA, Levin ES, Schweitzer PJ, Hardesty D.

Department of Psychiatry, Columbia University, New York, NY 10032, USA. baf1@columbia.edu

Lyme disease, caused by the bacterium Borrelia burgdorferi, can cause multi-systemic signs and symptoms, including peripheral and central nervous system disease. This review examines the evidence for and mechanisms of inflammation in neurologic Lyme disease, with a specific focus on the central nervous system, drawing upon human studies and controlled research with experimentally infected rhesus monkeys. Directions for future human research are suggested that may help to clarify the role of inflammation as a mediator of the chronic persistent symptoms experienced by some patients despite antibiotic treatment for neurologic Lyme disease.

PMID: 19944760 [PubMed - indexed for MEDLINE]


2. Nord J Psychiatry. 2008;62(5):386-91.

No association of seropositivity for anti-Borrelia IgG antibody with mental and physical complaints.

Grabe HJ, Spitzer C, Lüdemann J, Guertler L, Kramer A, John U, Freyberger HJ, Völzke H.

Department of Psychiatry and Psychotherapy, Ernst Moritz Arndt University Greifswald, Germany. grabeh@uni-greifswald.de

Undiagnosed chronic Lyme disease caused by Borrelia burgdorferi is considered a differential diagnoses in medically unexplained symptoms like arthralgias, distal paresthesias, depressive symptoms, lack of concentration and fatigue. The aims of the study were to assess the association of mental and physical complaints with seropositivity for anti-Borrelia IgG in a general population sample.

Seropositivity indicated an infection with Borrelia in the past. The Study of Health in Pomerania was conducted in a community living in a region with endemic Lyme disease. Mental and physical complaints were assessed on 38 items with the von Zerssen's complaint scale. IgG antibodies to Borrelia were determined by ELISA in 4264 individuals. Seropositivity was analyzed applying two cut-off scores (>5 and >10 IU/ml). IgG antibodies to Borrelia were found positive in 388 subjects (9.1%) applying the >5 IU/ml cut-off and in 130 subjects (3.0%) applying the >10 IU/ml cut-off. In multivariate analyses (MANCOVA), both definitions of seropositivity were not associated with increased mental or physical complaints while adjusting for gender, age, employment status, rural residency, physical activity, diabetes mellitus and number of chronic diseases. In the general population, seropositivity for anti-Borrelia IgG antibodies was not associated with an increase of self-rated mental or physical complaints or impairments. Therefore, clinicians should not overvalue seropositivity for anti-Borrelia IgG as a medical cause for unexplained mental or physical complaints.

PMID: 18752103 [PubMed - indexed for MEDLINE]


3. Med Hypotheses. 2008;70(5):967-74. Epub 2007 Nov 5.

The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders.

Bransfield RC, Wulfman JS, Harvey WT, Usman AI.

Department of Psychiatry, Riverview Medical Center, 225 State Route 35, Red Bank, NJ, United States. bransfield@comcast.net

Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders. A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life. Support for this hypothesis includes multiple cases of mothers with Lyme disease and children with autism spectrum disorders; fetal neurological abnormalities associated with tick-borne diseases; similarities between tick-borne diseases and autism spectrum disorder regarding symptoms, pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging data; positive reactivity in several studies with autistic spectrum disorder patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma; similar geographic distribution and improvement in autistic symptoms from antibiotic treatment. It is imperative to research these and all possible causes of autism spectrum disorders in order to prevent every preventable case and treat every treatable case until this disease has been eliminated from humanity.

PMID: 17980971 [PubMed - indexed for MEDLINE]


4. Int Psychogeriatr. 2005;17 Suppl 1:S65-77.

Dementia associated with infectious diseases.

Almeida OP, Lautenschlager NT.

University of Western Australia, School of Psychiatry and Clinical Neurosciences, Mail Delivery Point M573, 35 Stirling Highway, Crawley, Perth, WA 6009, Australia. osvalm@cyllene.uwa.edu.au

At the turn of the last century, infectious diseases represented an important cause of health morbidity and behavioral changes. Neurosyphilis, for example, was relatively common at the time and often led to the development of cognitive impairment and dementia. With the advent of effective antibiotic treatment, the association between infectious diseases and dementia became increasingly less frequent, although a resurgence of interest in this area has taken place during the past 15 years with the emergence of acquired immunodeficiency syndrome (AIDS) and variant Creutzfeldt-Jakob disease (vCJD). This paper reviews the most frequent infectious causes of dementia, including prion diseases, as well as infections caused by herpes virus, human immunodeficiency virus (HIV), toxoplasmosis, cryptococcus, cytomegalovirus, syphilis, borrelia and cysticercosis.

PMID: 16240484 [PubMed - indexed for MEDLINE]


5. Clin J Pain. 2005 Jul-Aug;21(4):362-3.

Painful hallucinations and somatic delusions in a patient with the possible diagnosis of neuroborreliosis.

Bär KJ, Jochum T, Häger F, Meissner W, Sauer H.

Department of Psychiatry, Friedrich-Schiller-University of Jena, Jena, Germany. karl-juergen.baer@med.uni-jena.de

Neuroborreliosis has become the most frequently recognized tick-borne infection of the nervous system in Europe and the United States. In addition to dermatological, cardiac, articular, and neurologic manifestations, psychiatric disorders such as depression, panic attacks, and schizophrenia-like psychosis can also arise. We report on a 61-year-old woman who developed a severe pain syndrome following several tick bites. She was diagnosed with neuroborreliosis; she received various courses of antibiotics over several years, but without any clinical improvement in her condition. Her eventual admission to a psychiatric ward due to mental symptoms and neuroleptic treatment led to a dramatic improvement of her pain symptoms. However, increasing delusions disclosed a psychotic episode, which ceased over time. We discuss therapeutic difficulties and psychiatric complications in the absence of a clear-cut diagnosis of neuroborreliosis. Although this patient might have suffered from late-onset schizophrenia with painful hallucinations right from the start of her disease, the case highlights psychiatric complications that might be associated with neuroborreliosis.

PMID: 15951656 [PubMed - indexed for MEDLINE]


6. Psychiatry Res. 2004 Dec 15;129(2):119-25.

Mycoplasma pneumoniae infection and Tourette's syndrome.

Müller N, Riedel M, Blendinger C, Oberle K, Jacobs E, Abele-Horn M.

Hospital for Psychiatry and Psychotherapy, Ludwig-Maximilians-University München, Nussbaumstrasse 7, D-80336 München, Germany. nmueller@psy.med.uni-muenchen.de

An association between infection and Tourette's syndrome (TS) has been described repeatedly. A role for streptococcal infection (PANDAS) has been established for several years, but the involvement of other infectious agents such as Borrelia Burgdorferi or Mycoplasma pneumoniae has only been described in single case reports. We examined antibody titers against M. pneumoniae and various types of antibodies by immunoblot in patients and in a sex- and age-matched comparison group. Participants comprised 29 TS patients and 29 controls. Antibody titers against M. pneumoniae were determined by microparticle agglutination (MAG) assay and confirmed by immunoblot. Elevated titers were found in significantly more TS patients than controls (17 vs. 1). Additionally, the number of IgA positive patients was significantly higher in the TS group than in the control group (9 vs. 1). A higher proportion of increased serum titers and especially of IgA antibodies suggests a role for M. pneumoniae in a subgroup of patients with TS and supports the finding of case reports implicating an acute or chronic infection with M. pneumoniae as one etiological agent for tics. An autoimmune reaction, however, has to be taken into account. In predisposed persons, infection with various agents including M. pneumoniae should be considered as at least an aggravating factor in TS.

PMID: 15590039 [PubMed - indexed for MEDLINE]


7. Neurology. 2003 Jun 24;60(12):1916-22.

Cognitive function in post-treatment Lyme disease: do additional antibiotics help?

Kaplan RF, Trevino RP, Johnson GM, Levy L, Dornbush R, Hu LT, Evans J, Weinstein A, Schmid CH, Klempner MS.

University of Connecticut School of Medicine, Farmington, USA. kaplan@psychiatry.uchc.edu

Comment in Neurology. 2003 Jun 24;60(12):1888-9.

BACKGROUND: It is controversial whether additional antibiotic treatment will improve cognitive function in patients with post-treatment chronic Lyme disease (PTCLD).

OBJECTIVE: To determine whether antibiotic therapy improves cognitive function in two randomized double-blind placebo-controlled studies of patients with PTCLD. METHODS: A total of 129 patients with a physician-documented history of Lyme disease from three study sites in the northeast United States were studied. Seventy-eight were seropositive for IgG antibodies against Borrelia burgdorferi, and 51 were seronegative. Patients in each group were randomly assigned to receive IV ceftriaxone 2 g daily for 30 days followed by oral doxycycline 200 mg daily for 60 days or matching IV and oral placebos. Assessments were made at 90 and 180 days after treatment. Symptom severity was measured from the cognitive functioning, pain, and role functioning scales of the Medical Outcomes Study (MOS). Memory, attention, and executive functioning were assessed using objective tests. Mood was assessed using the Beck Depression Inventory and Minnesota Multiphasic Personality Inventory.

RESULTS: There were no significant baseline differences between seropositive and seronegative groups. Both groups reported a high frequency of MOS symptoms, depression, and somatic complaints but had normal baseline neuropsychological test scores. The combined groups showed significant decreases in MOS symptoms, higher objective test scores, and improved mood between baseline and 90 days. However, there were no significant differences between those receiving antibiotics and placebo.

CONCLUSION: Patients with post-treatment chronic Lyme disease who have symptoms but show no evidence of persisting Borrelia infection do not show objective evidence of cognitive impairment. Additional antibiotic therapy was not more beneficial than administering placebo.

PMID: 12821733 [PubMed - indexed for MEDLINE]


8. Przegl Epidemiol. 2002;56 Suppl 1:37-50.

[Mental disorders in the course of lyme borreliosis and tick borne encephalitis].

[Article in Polish]

Juchnowicz D, Rudnik I, Czernikiewicz A, Zajkowska J, Pancewicz SA.

Klinika Psychiatrii AM w Białymstoku.

BACKGROUND: Lyme borreliosis is a chronic, multisystem disease, of prolong course with three consecutive stages, caused by a tick-transmitted spirochete Borrelia burgdorferi. Tick Borne Encephalitis (TBE) is neuroinfection caused by Tick Borne Encephalitis Virus (TBEV).

OBJECTIVE: We evaluated the occurrence of psychiatric manifestations in the early phase of borreliosis-erythema migrans and neuroboreliosis as well as in its late phase--in arthritis and in the Tick-Born Encephalitis. The aim of the study was to single out the most frequent psychiatric symptoms and psychopathological syndroms and to determine their dynamics.

METHODS: The study was carried out between 1999 and 2000 and comprised 174 patients of the Department of Psychiatry and Department of Infectious and Neuroinfectious Diseases of Medical Academy in Bialystok. Seventy seven patients diagnosed with arthritis, 20 with neuroborreliosis, 26 with skin manifestation-erythrema migrans and 51 with KZM participated. All subjects underwent psychiatric evaluation twice--during hospitalization and six month after discharge. Mental status examinations included general psychiatric examination and battery of scales and tests: Mini Mental State Examination, Beck Depression Inventory, Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Reitan's Trail Making Test, Choynowsky Memory Scale, Symptoms Inventory and neuropsychological testing.

RESULTS: Both in the course of TBE and Lyme borreliosis the majority of patients experienced psychiatric problems in the acute phase of disease as well as in the late phase--3, 6 months after the onset of the disease. The most common psychiatric manifestations were depressive disorders--episodes of depression or organic mood disorders, and cognitive deficits which manifest themselves as mild cognitive disorder or dementia.

CONCLUSION: Psychiatric assessment is important in early stage of kzm and borreliosis but first of all after termination of acute symptomatology.

PMID: 12194228 [PubMed - indexed for MEDLINE]


9. Psychiatr Pol. 1999 Mar-Apr;33(2):241-50.

[Neuroborreliosis: a psychiatric problem?].

[Article in Polish]

Popławska R, Szulc A, Zajkowska J, Pancewicz S.

Kliniki Chorób Psychicznych AM w Białymstoku.

The authors review the literature concerning clinical characteristics of neuroborreliosis with special focus on mental disorders. The patients develop mental disorders during the acute phase of the disease and even after several years. These disorders are often accompanied with various neurological syndromes. The authors discuss the most common mental disorders connected with neuroborreliosis: encephalopathy, cognitive disorders, dementia, depression, anxiety disorders. The paper describes the problem of neuroborreliosis in psychiatry, especially in the endemic regions.

PMID: 10786229 [PubMed - indexed for MEDLINE]


10. Appl Neuropsychol. 1999;6(1):12-8.

Relations among indexes of memory disturbance and depression in patients with Lyme borreliosis.

Barr WB, Rastogi R, Ravdin L, Hilton E.

Department of Neurology and Psychiatry, Long Island Jewish Medical Center, New Hyde Park, New York 11040, USA.

This study examined the relation between complaints of memory disturbance and measures of mood and memory functioning in 55 patients with serological evidence of late-stage Lyme Borreliosis (LB). Patients completed the Self-Ratings of Memory Questionnaire (SRMQ) and the Beck Depression Inventory. Memory functioning was assessed with the California Verbal Learning Test. Depressed patients exhibited more frequent complaints of memory disturbance on the SRMQ, although their pattern of responses did not differ from nondepressed patients. There was a significant correlation between subjective memory ratings and self-reported depression (Spearman rho = -.57, p < .001). No relation was observed between subjective memory ratings and objective memory performance. The results indicate subjective complaints of more severe memory disturbance in patients with LB and depression. Particular attention should be paid to the assessment of depression and subjective symptoms of memory disturbance when administering neuropsychological tests of memory functioning in patients with LB.

PMID: 10382566 [PubMed - indexed for MEDLINE]


11. Folia Neuropathol. 1999;37(1):43-51.

Central nervous system infection caused by Borrelia burgdorferi. Clinico-pathological correlation of three post-mortem cases.

Bertrand E, Szpak GM, Piłkowska E, Habib N, Lipczyńska-Lojkowska W, Rudnicka A, Tylewska-Wierzbanowska S, Kulczycki J.

Department of Neuropathology, Institute of Psychiatry and Neurology, Warszawa.

The spirochete Borrelia burgdorferi (B. burgdorferi) may cause severe meningoencephalomyelitis as the sole manifestation of Lyme borreliosis. We would like to present three such cases, where definite neuroborreliosis was clinically diagnosed in two cases and possible neuroborreliosis was recognized in one case. Alive spirochetes were isolated and cultured from blood and cerebrospinal fluid (CSF) in both definite cases. B. burgdorferi as the causative agent of the infection was confirmed in CSF by polymerase chain reaction (PCR) in one definite case. In the possible case spirochetes were cultured from blood and CSF. Alive spirochetes were not isolated, however anti-B. burgdorferi antibody value in serum was significantly elevated. On necropsy gross examination brain edema without focal changes was detected in two cases. Cerebral atrophy was seen in Case 3. Microscopically, lymphocytic infiltrates, microglial diffuse and nodular activation, spongiform changes, diffuse demyelination of the cerebral and cerebellar white matter, and diffuse astrocytosis, were characteristic pathological features in all presented cases. Multifocal, perivascular degenerative changes in the cerebral and cerebellar white matter were observed in the first case. Inflammatory changes in the nuclei and roots of cranial nerves were present in the third case.

PMID: 10337063 [PubMed - indexed for MEDLINE]


12. Psychiatr Clin North Am. 1998 Sep;21(3):693-703, viii.

The underdiagnosis of neuropsychiatric Lyme disease in children and adults.

Fallon BA, Kochevar JM, Gaito A, Nields JA.

Department of Psychiatry, Columbia University Medical Center, New York, New York, USA.

Lyme Disease has been called "The New Great Imitator," a replacement for that old "great imitator" neurosyphilis. This article reviews the numerous psychiatric and neurologic presentations found in adults and children. It then reviews the features of Lyme Disease, which makes it almost uniquely hard to diagnose, including the complexity and unreliability of serologic tests. Clinical examples follow that illustrate those presentations of this disease that mimic attention deficit hyperactivity disorder (ADHD), depression, and multiple sclerosis.

PMID: 9774805 [PubMed - indexed for MEDLINE]


13. Schizophr Res. 1997 Jun 20;25(3):177-81.

Schizophrenia, rheumatoid arthritis and natural resistance genes.

Rubinstein G.

Department of Psychiatry, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia.

The strong negative correlation between schizophrenia and rheumatoid arthritis might provide clues as to the aetiology of these two diseases. An immunological explanation has been sought in the HLA sector of the major histocompatibility complex, which has been shown to have a role in the development of rheumatoid arthritis. The search for an association between schizophrenia and HLA haplotypes, however, has yielded only controversial results. Nevertheless, an autoimmune aetiology is still suspected. The recent demonstration of geographical co-occurrence of high rates of schizophrenia and flavivirus infection suggests, for the first time, that a natural resistance gene (NRG) might be involved in the aetiology of schizophrenia. Such a NRG is carried by the C3H/RV mouse, providing protection against lethal infection by flavivirus, but not by the histocompatible C3H/He mouse. Furthermore, the C3H/He mouse has proved to be a good model for the development of Lyme arthritis, resulting from infection by Borrelia burgdorferi. It is suggested that there is a possibility that the C3H/RV mouse, which is known to be resistant to both flavivirus and rickettsia, may also be resistant to borrelia, since the Ixodid tick vector of flavivirus is the vector for all three of these organisms. If so, then the C3H/RV mouse would resist infection by borrelia, and could not develop Lyme arthritis. It is hypothesised, therefore, that despite the histocompatibility of these two strains, while the C3H/He mouse is vulnerable to Lyme arthritis, the C3H/RV mouse may be resistant. As a consequence, NRGs may play a part in triggering autoimmune disease, with HLA antigens responsible for its further development. This would indicate that the negative association of schizophrenia and rheumatoid arthritis could result from resistance or vulnerability to certain infections.

PMID: 9264173 [PubMed - indexed for MEDLINE]


14. Am J Psychiatry. 1994 Nov;151(11):1571-83.

Lyme disease: a neuropsychiatric illness.

Fallon BA, Nields JA.

Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York.

OBJECTIVE: Lyme disease is a multisystemic illness that can affect the central nervous system (CNS), causing neurologic and psychiatric symptoms. The goal of this article is to familiarize psychiatrists with this spirochetal illness.

METHOD: Relevant books, articles, and abstracts from academic conferences were perused, and additional articles were located through computerized searches and reference sections from published articles.

RESULTS: Up to 40% of patients with Lyme disease develop neurologic involvement of either the peripheral or central nervous system. Dissemination to the CNS can occur within the first few weeks after skin infection. Like syphilis, Lyme disease may have a latency period of months to years before symptoms of late infection emerge. Early signs include meningitis, encephalitis, cranial neuritis, and radiculoneuropathies. Later, encephalomyelitis and encephalopathy may occur. A broad range of psychiatric reactions have been associated with Lyme disease including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa, and obsessive-compulsive disorder. Depressive states among patients with late Lyme disease are fairly common, ranging across studies from 26% to 66%. The microbiology of Borrelia burgdorferi sheds light on why Lyme disease can be relapsing and remitting and why it can be refractory to normal immune surveillance and standard antibiotic regimens.

CONCLUSIONS: Psychiatrists who work in endemic areas need to include Lyme disease in the differential diagnosis of any atypical psychiatric disorder. Further research is needed to identify better laboratory tests and to determine the appropriate manner (intravenous or oral) and length (weeks or months) of treatment among patients with neuropsychiatric involvement.

PMID: 7943444 [PubMed - indexed for MEDLINE]


15. J Clin Psychiatry. 1993 Jul;54(7):263-8.

Psychiatric manifestations of Lyme borreliosis.

Fallon BA, Nields JA, Parsons B, Liebowitz MR, Klein DF.

Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY.

BACKGROUND: Lyme borreliosis (Lyme disease), a tick-borne spirochetal illness, has later manifestations that may include arthritic, neurologic, ophthalmologic, and cardiac symptoms. Recent reports suggest psychiatric symptoms may also be part of the clinical picture.

METHOD: Using a structured interview (SCID), we interviewed three patients who had developed a psychiatric disorder for the first time after infection with Borrelia burgdorferi.

RESULTS: During Lyme borreliosis, one patient had major depression and panic disorder, one patient had an organic mood syndrome with both depression and mania, and the third patient had panic disorder. These disorders remitted after adequate antibiotic treatment.

CONCLUSION: While depression has been previously linked to neuroborreliosis, this is the first report to link panic disorder and mania with borrelial infection. Because of the rapid rise of Lyme borreliosis nationwide and the need for antibiotic treatment to prevent severe neurologic damage, mental health professionals need to be aware of its possible psychiatric presentations.

PMID: 8335653 [PubMed - indexed for MEDLINE]


16. Fortschr Med. 1990 Apr 10;108(10):191-3, 197.

[Lyme borreliosis in neurology and psychiatry].

[Article in German]

Kohler J.

Neurologische Klinik mit Poliklinik, Universität Freiburg.

Neurological manifestations of Lyme disease are as multifarious as the entire spectrum of this common infection. In stage I, fibromyalgia and, more rarely, painful muscular fasciculation, dominate the clinical picture. In the individual case, mild psychic abnormalities may already be observed. Characteristic of the 2nd stage is lymphocytic meningopolyneuritis. Involvements of the CNS are expressed not so much in focal deficits, as in diffuse psychopathological disorders. In stage 3, CNS manifestations are characterized by chronic, in part multifocal, encephalitides and encephalomyelitides, isolated transverse myelitides and cerebral vasculitic disorders. The clinical symptomatology may be dominated by severe psychiatric syndromes. Connatal and subclinical latent infections of the nervous system with Borrelia represent special forms.

PMID: 2187778 [PubMed - indexed for MEDLINE]


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