The Neuropsychiatric Assessment of Lyme Disease

Medical topics with questions, information and discussion related to Lyme disease and other tick-borne diseases.
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 3 Nov 2007 11:26

Med Mal Infect. 2007 Mar 15; [Epub ahead of print] Links
[Clinical manifestations and epidemiological aspects leading to a diagnosis of Lyme borreliosis: neurological and psychiatric manifestations in the course of Lyme borreliosis.][Article in French]


Créange A.
Service de neurologie, centre hospitalier universitaire Henri-Mondor, APHP, université Paris-XII, 94000 Créteil, France.

Lyme disease is associated with various systemic and neurological manifestations. The neurological and psychiatric manifestations of Lyme disease are more frequently observed during its secondary phase (stage 2) than during its late tertiary phase (stage 3). In stage 2, cerebrospinal fluid and bacterial tests are consistent with the ongoing infection. Painful meningoradiculitis, encephalomyelitis and encephalitis, and symptoms of depression are the most characteristic at this stage. The diagnosis should be based on the association of clinical, epidemiological, and biological features. Adequate treatment usually leads to recovery. In stage 3 of the disease, the link between neurological manifestations and initial infection is uncertain. Distal axonal polyneuropathy and chronic encephalopathy are the most frequently reported presentations.

PMID: 17368785
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 3 Nov 2007 11:29

The "Other Side" of Lyme Disease: Understanding -- and Overcoming -- Lyme's Psychological Symptoms

Advanced cases of Lyme disease can cause psychological and cognitive problems. These symptoms can include intense mood swings, irritability, depression and anxiety, memory loss, slowed cognitive processing, diminished concentration, problems with reading and speaking, spatial disorientation, and cognitive discontinuity.

Greenwich (PRWEB) October 18, 2007 -- By now, everybody's heard of Lyme disease -- with approximately 20,000 new cases reported each year, it's the most common vector-borne disease in the United States. We've heard about the tell-tale "bull's eye" rash that often develops at the site of a bite from an infected tick, and probably know about the more common symptoms of a Lyme infection, including fever, aching joints, fatigue and headaches.

But what most people don't know is that an advanced case of Lyme disease can cause psychological and cognitive problems, as well, says Diane Blanchard, co-president and co- founder of Time for Lyme, Inc., a research, education and advocacy group, which along with the Lyme Disease Association, recently endowed the first Lyme and Tick-Borne Diseases Research Center at Columbia University Medical in NYC dedicated to the study of chronic Lyme disease. These symptoms can include intense mood swings, irritability, depression and anxiety, memory loss, slowed cognitive processing, diminished concentration, problems with reading and speaking, spatial disorientation, and cognitive discontinuity (losing track of a conversation or train of thought). Complicating matters further, the symptoms can be intermittent and vary from day to day.

"Patients with advanced Lyme disease can also have problems multi-tasking," Blanchard says. "They say they've got 'brain fog,' which keeps them from thinking and speaking clearly." Some patients also report a kind of cognitive "short-circuiting" that makes them feel confused, lose focus, stutter, or panic.

Unfortunately, patients often don't understand the root of these symptoms, says Mindy Beth Lipson, Psy.D., a psychologist in New Rochelle, NY and recently appointed Time For Lyme Advisory Board member, who frequently works with Lyme disease patients and leads Time for Lyme's patient support group (sponsored by Time for Lyme, Greenwich Hospital and the Greenwich Deptartment of Health). To make things worse, many doctors don't understand them, either. "Lyme disease is a multi-system illness," she explains. "The bacteria that cause Lyme have been found in all areas of the human body, including the brain." Lyme disease is similar to Syphilis, which was also dubbed "The Great Imitator" because it has the same properties -- and the same ability to mimic a multitude of illnesses. "If a Lyme infection is left uncontrolled, it can do a great deal of damage," Dr. Lipson says. "Unfortunately, the damage is often mistaken for that caused by other disease processes
Psychological and cognitive problems often develop a year or more after infection, and are much more problematic in people whose Lyme disease wasn't treated adequately -- or treated at all -- at its onset. Although Lyme disease responds well when diagnosed and treated early, patients don't always see the tick (or the rash), and doctors can sometimes miss a diagnosis, as well. These patients are at risk of developing a chronic form of Lyme disease, which can bring with it a host of psychological, cognitive and other problems. And right now, there is no consensus in the medical community as to how best to treat patients with the later stages of the disease.

The Psychological Toll
Patients suffering from the psychological and cognitive symptoms of advanced Lyme disease (also known as late neuropsychiatric Lyme disease) are also facing a slew of other problems, Dr. Lipson says. The stress can create or exacerbate an inability to work, and financial, marital or relationship problems can develop, as can frequent feelings of isolation and fears about the future. All of this can contribute to depression and anxiety.

Dr. Lipson notes that, for depression and anxiety, antidepressant medications can be helpful, as can learning coping strategies and effective communication skills to help deal with family, friends, and medical providers. She also recommends seeking out a specialist trained in medical or health psychology, such as a medical or health psychologist, ideally someone who's treated other patients with Lyme disease.

http://www.prweb.com/releases/2007/10/prweb561780.htm
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 3 Nov 2007 11:32

Worsening of Symptoms During Antibiotic Treatment

Nearly half of the patients in our sample reported a transient worsening of neuropsychiatric symptoms during the first few days of antibiotic treatment. The worsening of symptoms during initiation of antibiotic treatment is thought to be a variant of the Herxheimer reaction as seen in the treatment of syphilis (33). In Lyme disease, however, this Herxheimer-like reaction can be quite prolonged-lasting a few days or longer-and can be frightening to patients who are expecting a resolution, not a worsening, of their symptoms. The reaction can sometimes be difficult to distinguish from an allergic reaction to the medicine, a distinction with obvious and crucial treatment implications.

This Herxheimer-like reaction may be experienced as a worsening of psychiatric symptoms: some patients in our sample experienced panic attacks for the first and only time when starting on antibiotics. Others have reported an intensification of depressive symptoms, suicidality or anxiety. Many reported an increased startle response and photophobia during the first few days of antibiotic treatment.



http://www.geocities.com/playpub/AR-NB- ... c119817522
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sun 16 Dec 2007 10:32

Lyme Disease, Comorbid Tick-Borne Diseases, and Neuropsychiatric Disorders

Robert C. Bransfield, MD

Many recall the phrase "To know syphilis is to know medicine." Now Lyme disease (Lyme borreliosis), the new "great imitator,"1 is the ultimate challenge to the breadth and depth of our knowledge. In psychiatry, we generally treat mental symptoms or syndromes rather than the underlying cause of a disorder. A greater awareness of immune reactions to infections and other contributors to mental illness enhances our psychiatric capabilities. Lyme disease, like syphilis, is caused by a spirochete with a multitude of pos-sible manifestations and 3 stages: early with dermatological symptoms, disseminated, and late stage.

Unlike Treponema pallidum, the cause of syphilis, the causative agent of Lyme disease, Borrelia burgdorferi, can be much more difficult to eliminate, diagnostic testing is less reliable, and interactive copathogens are major contributors in the pathophysiology.2,3 B burgdorferi is highly adaptable with 6 times as many genes as T pallidum and 3 times as many plasmids as any other bacteria that allow rapid genetic adaptations.4,5 It is a stealth pathogen that can evade the immune system and pathophysiological mechanisms.6,7 Knowingly or not, most psychiatrists have at some point been perplexed by patients with late-stage psychiatric manifestations of Lyme borreliosis. Several factors are associated with the risk of infection as well as the different manifestations of Lyme borreliosis (Table 1).

A problematic case
The following composite case illustrates a number of problems that may make diagnosis and treatment of Lyme borreliosis anything but straightforward. The patient is in good health and enjoys outdoor activities. Often this person has the HLA DR4 genotype. He or she may acquire a small tick bite that goes unnoticed because the subsequent rash may not be of the classic bull's-eye type, may be easily overlooked in dark-skinned individuals, may be misdiagnosed, or may occur only with a second or subsequent infection. There may be flu-like symptoms with migratory musculoskeletal aches and pains. If a diagnosis of Lyme disease is made, the initial course of antibiotic treatment may not have been sufficient to eliminate the infection. (Although standardized by 1 set of guidelines, psychiatrists often see the failures of some of the "standard" treatments.) Low-grade symptoms may remit and periodically relapse over time. An accident, emotional stress, vaccination, or childbirth can trigger an exacerbation of symptoms.

The patient, who did not have psychosomatic symptoms and was not hypochondriacal in the past, now complains of an increasing number of somatic, cognitive, neurological, and psychiatric symptoms. Although Lyme disease may be suspected, the laboratory tests available to most clinicians often lack sensitivity and thus are read as negative for Lyme disease. Fibromyalgia, chronic fatigue syndrome, or multiple sclerosis (MS) may be erroneously diagnosed.

Treatment of some symptoms with corticosteroids may initially provide relief, but a more rapid decline often follows. The patient sees multiple specialists, each of whom restricts the examination to his area of expertise. Nothing is resolved, and the patient is frustrated that his symptoms cannot be explained. In view of the growing list of unexplained symptoms, including psychiatric symptoms, the patient is treated with tranquilizers and antidepressants with some benefit, but gradual decline persists.

The major complaints include fatigue, multiple cognitive impairments, depression, anxiety, irritability, head-aches, and a multitude of other symptoms. When general medical treatment fails, the patient may be referred to a psychiatrist for 3 reasons: the unexplained medical symptoms give the appearance of a psychosomatic or somatoform condition; complex mental symptoms are thought to require psychiatric assessment; and a psychiatrist is thought to be needed to more effectively manage psychiatric treatments.

The Figure presents single photon emission CT (SPECT) images of the brain of a depressed 51-year-old woman with Lyme disease, before and after treatment with ceftriaxone. She walked on nature trails at home and on vacations, recalled frequent tick bites and an expanding bull's-eye rash on her abdomen with no other symptoms, but considered it of no special significance at the time. Over 8 years, there was a progressive development of unexplained symptoms that began with GI complaints, followed by cognitive impairment, fatigue, depression, arthritis, and shortness of breath. The primary diagnosis was atypical depression. Although the patient failed to respond to 51 different drug trials, the treating psychopharmacologist assured her the mental symptoms could not possibly be caused by an underlying physical condition.

The initial SPECT scan demonstrated "extensive hypoperfusion... predominantly in the frontal and temporal lobes and to a less degree in the parietal and occipital lobes," which is consistent with Lyme disease and neurodysfunction. Neurocognitive testing demonstrated significant abnormalities. An MRI scan ruled out frontal temporal dementia. The patient tested negative for Lyme disease by CDC epidemiological criteria, but the Lyme IgG Western blot test result was positive at one laboratory and equivocal at another. The CD57 lymphocyte count was low at 17/µL (60 to 360) and the patient tested positive for 4 other tick-borne infections (Mycoplasma fermentans, Babesia microti, Babesia WA-1, and Bartonella henselae). The patient was intolerant to oral antibiotics and was treated with 8 months of intravenous ceftriaxone. The second SPECT scan demonstrated "marked improvement of the hypoperfusion pattern in the temporal, frontal, and parietal lobes and small areas of hypoperfusion pattern remain." The depression never returned, but some mild residual symptoms persist,
including fatigue, neuropathy, and arthritis; however, she has mostly returned to her active lifestyle. The failure to diagnose and treat these infections for several years resulted in an escalation of symptoms and a loss 8 years of her life that could have been prevented by earlier diagnosis and treatment.

General theoretical issues

The causes of most psychiatric illnesses are unknown. The catecholamine hypothesis does not adequately explain the cause of abnormal neurotransmitter functioning. Mendel stated that human traits are determined by individual genes that function independently of other genes and environmental influences. Koch believed that many human diseases are caused by microbes that exert their effect independently of other microbes, environmental factors, and genes. The cause of most mental illnesses cannot be explained by neurotransmitters, genes, or infections alone. Instead, as stated by Yolken,8

most common human diseases are caused by the interaction of environmental insults and susceptibility genes.Many of the susceptibility genes are diverse determinants of human response to environmental factors, including infections, and prevention or treatment of the infections may result in the effective treatment of complex disorders.

Neuropsychiatric disease is often associated with an interaction of environmental insults and susceptibility factors that frequently results in a pathological interaction including inflammation, oxidative stress, mitochondrial dysfunction, and excitotoxicity, which leads to neuronal dysfunction.3

Numerous studies document that infections, such as pediatric autoimmune
neuropsychiatric disorders associated with streptococcal infections, syphilis, hepatitis C, and zoonotic (animal) diseases, can cause mental illness.9-13 The same syndrome may be caused by different infections in different individuals, and the same infection can cause different syndromes in different individuals. For example, obsessive-compulsive disorder has been caused by infection with Streptococcus, B burgdorferi, Japanese B encephalitis virus, herpes simplex virus 1, Borna disease virus, Epstein-Barr virus, and Mycoplasma, as well as by thepandemic influenza of 191814-16; I have also observed cases caused by Hong Kong influenza and coxsackievirus infection. Of course, many of these infections have also been shown to cause other psychiatric and somatic symptoms. Some infections result in residual injury even after the infection itself no longer persists, while other infections may persist in a chronic relapsing and remitting state. Chronic infections are most commonly viral, venereal, and vector-borne zoonotic.8

Tick-borne diseases and chronic infectious diseases
B burgdorferi, the principal organism associated with Lyme borreliosis, is one of the most complex bacteria known to man. In addition, a tick bite can presumably transmit more than 1 disease-causing organism. Thus, 2 major clinical hurdles in diagnosis and management are the absence of a clear therapeutic end point in treating Lyme borreliosis and the potential presence of tick-borne coinfections that may complicate the course of the illness.3 The more common interactive coinfections may be caused by M fermentans, Mycoplasma pneumoniae, B microti, Ba- besia WA-1, Chlamydia pneumoniae, Ehrlichia, Anaplasma, and B henselae, and multiple viruses and fungi.2,3,17 When multiple microbes grow together, they can promote immunosuppressive effects and cause marked symbiotic changes that alter their functioning.18

Neuroborreliosis is an infection within the brain; however, infections in the body that do not pass through the blood-brain barrier may also impact the brain indirectly via immune effects. All the clinical manifestations, acute or chronic, of infection with B burgdorferi are characterized by strong inflammation with the production of several proinflammatory and anti-inflammatory cytokineswith an aberrant innate proinflammatory response19 and inflammatory brain changes.20 Most of the dysfunction caused by these infections is associated with immune reactions.

Lyme borreliosis and other tick-borne infections are associated with a combination of inflammatory reactions and autoimmune symptoms. The proinflammatory cytokines associated with these infections increase indoleamine 2,3-dioxygenase, which decreases serotonin and kynurenic acid, a neuroprotective glutamate antagonist. In addition, the cytokines increase the level ofquinolinic acid, an N-methyl d-aspartic acid (NMDA) agonist and neurotoxin, which contributes to the neurological and cognitive deficits seen in patients with tick-borne infections.21-23 This change may produce over-stimulation of hippocampal (NMDA) receptors leading to apoptosis and hippocampal atrophy. Hippocampal atrophy in the temporal lobes caused by NMDA overstimulation has been associated with depression and dementia.24


Lyme borreliosis and other tick-borne infections can exist as an asymptomatic chronic carrier state, they can present with occasional or chronic fluctuating low-level symptoms, or they can lead to severe multisystem dysfunction and a multitude of psychiatric presentations

http://www.psychiatrictimes.com/showArt ... 91&CID=rss
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Fri 28 Dec 2007 21:36

Lyme neuroborreliosis presenting chiefly with neuropsychiatric symptoms displaying difficulties in diagnosis: Report of two cases


Hayrettin Akdeniz A1, Lütfullah Beşiro&gcaron;lu A2, Hasan Karsen A1, M. Kasım Karahocagil A1, Mehmet Yücel A&gcaron;argün A2

A1 Yüzüncü Yıl University, Faculty of Medicine, Department of Infectious Diseases, Van, Turkiye
A2 Yüzüncü Yıl University, Faculty of Medicine, Department of Psychiatry, Van, Turkiye


Abstract:


Lyme disease is an infectious disease caused by the tick-borne spirochete Borrelia burgdorferi. Its clinical hallmark, erythema migrans, is present only in about two thirds of infected patients. After erythema migrans, Bannwarth's syndrome (meningitis, polyradiculoneuritis, cranial nerve palsies) represents the second most common clinical manifestation of acute Borrelia infection, especially in Europe. We describe here two cases of Lyme neuroborreliosis presenting chiefly with neuropsychiatric symptoms displaying difficulties in diagnosis because the patients had no history of tick bite or erythema migrans. In one of the cases, psychiatric complaints were predominant and she had a preliminary diagnosis of catatonic and psychotic disorder due to a general medical condition. The other patient had a clinical picture of meningitis with a protracted course. They were successfully treated with oral doxycycline. Apropos of these two cases, the relevant literature has been reviewed.

iospress.metapress.com/index/7T5HURWKCK7L7MUU.pdf
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 12 Jan 2008 23:41

Psychiatr Pol. 1999 Mar-Apr;33(2):241-50.Links
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
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 12 Jan 2008 23:42

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

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
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Fri 18 Jan 2008 10:07

Nervenarzt. 1991 Aug;62(8):514-5. Links

Subacute organic psychosyndrome as a clinical manifestation of infection with stage II Borrelia burgdorferi without further neurologic manifestations
[Article in German]


Reess J, Mauch E, Kornhuber HH.
Fachklinik für Neurologie Dietenbronn, Schwendi.

A 60-year old man developed a subacute psychoorganic syndrome over four weeks. CCT was normal, except a slight atrophy of the cerebellar superior vermiform process. In the CSF we found 1696/3 cells, suggesting a lesion of the hemato-encephalic barrier, an autochthonous IgG production and an increased specific antibody-titre (10.3) for Borrelia burgdorferi. Based on these data a Lyme-Neuroborreliosis being diagnosed. Treatment with Cefotaxim and Gentamycin was successful, a complete remission of the psychopathological symptoms had been obtained. This case is an uncommon manifestation of a Borrelia-burgdorferi-infection of the CNS with psychopathological symptoms but no neurological deficit. We conclude that an affection of the CNS with Borrelia burgdorferi must always be taken into consideration in patients presenting a subacute psychoorganic syndrome of unknown etiology.

PMID: 1944717
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Sat 19 Jan 2008 10:59

J Neurol. 1992 Mar;239(3):129-31. Links

Untreated neuroborreliosis: Bannwarth's syndrome evolving into acute schizophrenia-like psychosis. A case report.
Roelcke U, Barnett W, Wilder-Smith E, Sigmund D, Hacke W.
Neurologische Klinik, Universität, Heidelberg, Federal Republic of Germany.

In general, meningopolyradiculitis (Bannwarth's syndrome, stage 2 of neuroborreliosis) follows a predictable monophasic self-limiting course. In contrast, we report the case of a patient with an untreated meningopolyradiculitis which evolved into acute schizophrenia-like psychosis due to persistent infection with Borrelia burgdorferi. The psychosis resolved within 1 week of treatment with ceftriaxone. This case shows that the usually benign monophasic meningopolyradiculitis may progress to severe CNS complications, which may have implications on current pathophysiological beliefs.

PMID: 1573415
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Re: The Neuropsychiatric Assessment of Lyme Disease

Post by Yvonne » Mon 3 Mar 2008 15:08

Windows to the Brain

Acute and Chronic Lyme Disease: Controversies for Neuropsychiatry

Robin A. Hurley, M.D. and Katherine H. Taber, Ph.D

In conclusion, tick-borne diseases have been identified since the early 20th century. The last 20 years have brought a more complete picture of the most commonly presenting acute tic-borne illnesses. Diagnostic triads and treatment recommendations have been published. More controversial are the answers to those patients who develop nonspecific and lingering neuropsychiatric symptoms postinfection. Questions remain as to whether or not these symptoms are a direct result of continued hidden infection or a result of a different secondary process (e.g., psychological reaction, inflammatory cascade induction, autoimmune). It is, however, prudent for the practicing clinician to be aware of Lyme disease in the differential for patients with new-onset neuropsychiatric symptoms in an endemic area. Awareness is particularly necessary if the patient also has an absence of a known psychiatric history, presence of fatigue and/or chronic musculoskeletal pain, nonspecific inflammatory white matter disease on standard imaging or hypometabolism/hypoperfusion on functional imaging.

http://neuro.psychiatryonline.org/cgi/c ... 1/iv?ct=ct
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