Näiden tutkimusten perusteella Ljøstad ja Mygland tulivat siihen tulokseen että nykyisillä diagnostisilla menetelmillä he eivät löytäneet mitään todistetta meneillään olevasta borrelia-infektiosta. Siitä huolimatta 48%:lla oli positiivinen vasta-ainetestitulos ja 72%:lla tuntemattomasta syystä johtuvia oireita. Loppujen oireiden syyksi ilmoitettiin jokin muu tunnettu sairaus. Sairastuneilla esiintyi normaalia enemmän fatiikkia, elämänlaadun heikkenemistä oireiden vuoksi. Henkilöt eivät olleet muita luulotautisempia, masentuneempia tai ahdistuneempia.
Eur J Neurol 2012(Mar)
The phenomenon of 'chronic Lyme'; an observational study.
Ljøstad U, Mygland A
Department of Neurology, Sørlandet Hospital, Kristiansand, Norway Institute of Clinical Medicine, University of Bergen, Bergen, Norway Department of Habilitation, Sørlandet Hospital, Kristiansand, Norway.
# DOI: 10.1111/j.1468-1331.2012.03691.x
Purposes: To chart clinical, laboratory, and psychometric profiles in patients who attribute their complaints to chronic Lyme disease.
Methods: We assessed the patients by clinical examination, laboratory tests, and questionnaires measuring fatigue, depression, anxiety, health-related quality of life, hypochondriasis, and illness perceptions.
Mielenkiintoinen tulkinta norjalaisilta.
Results: We found no evidence of ongoing Borrelia burgdorferi (Bb) infection in any of the 29 included patients using current diagnostic guidelines and an extended array of tests. Eight (28%) had other well-defined illnesses. Twenty-one (72%) had symptoms of unknown cause, of those six met the suggested criteria for post-Lyme disease syndrome. Fourteen (48%) had presence of anti-Bb antibodies. The patients had more fatigue and poorer health-related quality of life as compared to normative data, but were not more depressed, anxious, or hypochondriacal. Their beliefs about the illness were characterized by negative expectations.
Conclusion: Our patients, who all attributed their symptoms to chronic Lyme disease, were heterogeneous. None had evidences of persistent Bb infection, but whether current diagnostic criteria are functional in patients with longstanding complaints is controversial. Other well-defined illnesses or sequelae from earlier Lyme disease were probable as main explanatory factor in some cases. The patients were not more depressed, anxious, or hypochondriacal than the normal population, but they had poorer health-related quality of life, more fatigue, and negative expectations about their illness.
© 2012 The Author(s). European Journal of Neurology © 2012 EFNS.
http://www.familypracticenews.com/news/ ... 578d5.html
Lyme Disease Presents Differently in Men and Women
By: SHARON WORCESTER, Family Practice News Digital Network
ATLANTA ? Women with Lyme disease display more clinical symptoms than do men with the disease and also are less likely to seroconvert following treatment, according to findings from a prospective cohort study involving 77 patients.
Numerous symptoms were reported more often by the 37 women in the study than by the 40 men. For example, significantly more women than men reported joint pain, muscle pain, headache, back pain, heart palpitations, nausea, vomiting, anxiety, numbness and tingling, and changes in vision during at least one of six preplanned study visits with a physician, Lauren A. Crowder, M.P.H. reported in a poster at the International Conference on Emerging Infectious Diseases.
Photo courtesy Janice Haney Carr/CDC
One hypothesis for the differences between men and women in terms of Lyme disease symptoms is that there may be an immunological variation in response to Borrelia burgdorferi (shown here), the bacterial infection that causes Lyme disease.
Joint pain, heart palpitations, nausea, vomiting, and changes in vision were reported significantly more often by women at two of the six visits, and headache was reported significantly more often by women at four of the six visits.
"The second preliminary finding we observed in our cohort of patients was that women were less likely to seroconvert on the antibody tests for serodiagnosis of Lyme disease," Ms. Crowder of the Lyme Disease Research Foundation, Lutherville, Md., said in an interview.
At the initial study visit, a similar proportion of men and women (about 60% of each) tested negative for Lyme disease using the Centers for Disease Control and Prevention?s recommended two-tier testing criteria for serodiagnosis. However, at the second visit, which was performed immediately post treatment, 70% of women who tested negative at the first visit remained negative, compared with only 35% of the men who initially tested negative.
Additionally, polychromatic flow cytometry performed on patient samples indicated that women had significantly higher frequency of CD4+CCR5+ T-cells prior to treatment than did men (mean of 9.82% vs. 5.96%).
"These findings suggest to us that there may be a difference between how men and women respond to infection with Lyme disease. One hypothesis for these differences is that there may be an immunological variation in response to Borrelia burgdorferi, the bacterial infection that causes Lyme disease, between men and women," Ms. Crowder said.
Study participants had early, untreated erythema migrans and clinically confirmed Lyme disease. At the first of the six study visits, they were tested using the CDC criteria by a commercial laboratory. All were treated with 3-week course of doxycycline and were then followed for up to 2 years. At each study visit, participants underwent a physical examination and interval history, reported clinical symptoms and completed self-administered surveys, and underwent repeat laboratory evaluations.
The findings highlight a need for additional research on sex-based differences in the effects of early Lyme disease. Such differences have been seen in other infectious disease, but have not been thoroughly explored in early Lyme disease, Ms. Crowder noted.
Eur J Heart Fail 2012(Feb)
Detection of Borrelia burgdorferi sensu lato in endomyocardial biopsy specimens in individuals with recent-onset dilated cardiomyopathy.
Kubánek M, Sramko M, Berenová D, Hulínská D, Hrbácková H, Malusková J, Lodererová A, Málek I, Kautzner J
Department of Cardiology, Institute for Clinical and Experimental Medicine, Videňská 1958/9, Prague, Czech Republic.
# DOI: 10.1093/eurjhf/hfs027
AIMS: Recent studies in patients with dilated cardiomyopathy (DCM) have detected the genome of Borrelia burgdorferi sensu lato (BBSL) in endomyocardial biopsy (EMB) specimens using a qualitative polymerase chain reaction (PCR), suggesting a causal link between Lyme disease and DCM in areas in which Lyme disease is endemic. We aimed to study this relationship using a comprehensive molecular analysis detecting BBSL in EMB samples.
METHODS AND RESULTS: We performed a comprehensive histopathological, immunohistochemical, ultrastructural, and molecular analysis targeting cardiotropic viruses and BBSL in EMB specimens of 41 individuals with recent-onset DCM and 15 controls with end-stage coronary artery disease. Specifically, quantitative PCR and electron microscopy of EMB specimens were employed. In addition, autoantibodies and manifestation of autoimmune diseases were evaluated in both groups. Individuals with recent-onset DCM presented more frequently with myocar dial BBSL persistence as compared with the control group (24% vs. 0%, P = 0.035). In contrast, the prevalence of parvovirus B19 and cytomegalovirus was similar in both groups. Sequence analysis of borrelial DNA revealed the following genospecies: Borrelia burgdorferi sensu stricto in three patients (30%), Borrelia afzelii in two patients (20%), and Borrelia garinii in four patients (40%), the results being inconclusive in one case. BBSL-positive DCM patients had a higher prevalence of organ-specific autoimmune diseases in comparison with the remaining DCM patients (50% vs. 16%, P = 0.030).
CONCLUSION: Myocardial persistence of BBSL may be involved in the pathophysiology of DCM in individuals living in areas in which Lyme disease is endemic.
Rev Med Interne 2012(Feb)
[Lyme disease with hepatitis and corticosteroids: A case report.]
Muslmani M, Gilson M, Sudre A, Juvin R, Gaudin P
Service de rhumatologie, hôpital Sud Échirolles, CHU de Grenoble, avenue Kimberley, 38130 Échirolles, France.
# DOI: 10.1016/j.revmed.2012.01.016
INTRODUCTION: Abnormalities of liver function tests have been occasionally described in large series of Lyme disease, but only one case of hepatitis directly related to infection have been described in literature.
CASE REPORT: A 78-year-old-man, with a past medical history of polymyalgia rheumatica (PMR) who had discontinued corticosteroids two years before, presented a transient acute fever and liver cholestasis and cytolysis after an exposure to tick bites. A few days later, cervical pain occurred and corticosteroids were resumed as a PMR relapse was suspected. Hematogenous dissemination with acute meningoradiculitis and multiple erythema migrans led to conclude to a stage 2 Lyme disease.
CONCLUSION: Although hepatitis complicating the course of Lyme disease has been described in literature, the marked inflammation in our patient led us to investigate the possibility of a co-infection. Also, we discuss the responsibility of corticosteroids in clinical worsening of Lyme disease if they are prescribed without concomitant antibiotics.
Copyright Â© 2012 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.
Med Hypotheses. 2005;64(4):717-20.
Is Gulf War Syndrome actually chronic Lyme disease?
Department of Accident and Emergency, College of Medicine, University of Wales, Heath Park, Cardiff United Kingdom, Cardiff, UK.
Symptoms of Gulf War Syndrome and chronic Lyme disease are very similar. Lyme disease is a condition which can be difficult to diagnose since one of the main features of the condition, the erythema migrans rash, may be absent or overlooked and serological testing for Lyme disease may be falsely negative. Symptoms of Lyme disease may not became apparent until years after exposure to the causative organism. Military personnel during training in the field are at risk of tick bites and it may be that those who developed Gulf War Syndrome entered the conflict with latent Lyme disease. There has been no systematic examination of Gulf War Syndrome sufferers for chronic Lyme disease and it is hypothesized that chronic Lyme disease has been overlooked as a cause of Gulf War Syndrome. To address this it is suggested that sufferers of Gulf War Syndrome or similar illnesses should be examined by physicians who have experience diagnosing and treating large numbers of patients with Lyme disease.
PMID: 15694687 [PubMed - in process]
Ultraäänitutkimusta voidaan käyttää Borrelioosin seurantaan mutta se ei erotusdiagnostiikkaan kovin hyvin. (2012)
Int J Infect Dis 2012(Jan)
Ultrasonographic evaluation of knee joints in patients with Lyme disease.
Czupryna P, Moniuszko A, Czeczuga A, Pancewicz S, Zajkowska J
Department of Infectious Diseases and Neuroinfections, Medical University in Białystok, Żurawia Street 14, 15-540 Białystok, Poland.
# DOI: 10.1016/j.ijid.2011.12.004
OBJECTIVE: The aim of this study was to evaluate the ultrasonographic images of patients with chronic knee pain and serologic features of Lyme disease.
METHODS: Seventy-six patients hospitalized in The Department of Infectious Diseases and Neuroinfections of the Medical University in Białystok, Poland were included in the study. Patients were divided into two groups: (1) the Lyme disease group included patients with pain in one or both knees and anti-Borrelia burgdorferi antibodies with symptoms lasting for over 6 months; (2) the control group included patients suffering from pain in one or both knees for over 6 months, but for whom B. burgdorferi infection was excluded.
RESULTS: The most frequent ultrasonographic finding in the Lyme disease group was effusion, and its frequency was significantly higher than in the control group. No patient in the control group presented with synovitis or cartilage damage, while these were quite frequent findings in the Lyme disease group. Baker's cysts were more frequent in the Lyme disease group, but this was statistically non-significant.
CONCLUSIONS: Ultrasonography may be useful in following the sequelae of Lyme disease. The abnormalities found in Lyme disease patients are non-specific and ultrasonography is not useful in the differential diagnosis.
Copyright © 2012 International Society for Infectious Diseases.
Published by Elsevier Ltd. All rights reserved.
HYPERACUSIS AND LYME DISEASE
Lyme disease patients can experience an extreme sensitivity to sound, also known as auditory hyperacusis. In some patients it is limited to louder sounds, but in the more severe cases "ordinary" sounds can be very debilitating. The impact can be felt throughout the body, and this condition can affect every aspect of daily living. Patients can experience heightened awareness and an inability to tolerate conversation, running water, page turning, the humming of electronic devices, other people's breathing, etc. These normal everyday sounds become painful and unbearable, and as a result the individual's ability to leave the home is greatly limited. Patients may also experience an increased startle response and an "electric shock" type feeling.
Sounds can also induce dizziness, and this is called Tullio's phenomenon or audiogenic seizure disorder. According to Jenifer Nields, MD, "This peculiar short-circuiting of the inner ear's auditory and vestibular functions is known as the Tullio phenomenon. This phenomenon has been deemed pathognomonic for syphilis (43) but, as it appears, can occur in Lyme disease as well (41), and thus provides one more example of the "new great imitator," Lyme disease, imitating the old "great imitator," syphilis (1)." (Psychiatric Quarterly, Spring 1992). Vestibular Hyperacusis can also affect the autonomic nervous system.
Sometimes another central auditory processing disorder, tinnitus (buzzing or ringing in the ear), can accompany hyperacusis. Lyme disease patients can also experience sensitivities to light, smells, taste, touch, motion and/or temperatures.
The best treatment is often determined based on trial and error, and the results vary from patient to patient. Treatment can include a combination of sound avoidance, sound reduction devices, tinnitus retraining, relaxation, medication and nutrients. The use of ear protection is an individual decision and can be complicated. On the one hand ear plugs can cause a vicious cycle where the brain adjusts and becomes even less tolerant to noises, but on the other hand some may find it absolutely necessary. Some patients like ear plugs, but others prefer headphones such as Shooter's or Bose. For various reasons, some patients may not tolerate ear protection at all and find it creates other problems.
It is important to discuss all treatment options with your physician. In the case of Lyme disease, hyperacusis may or may not resolve or reduce with antibiotic treatment, and other treatments may also be necessary. There are some psychiatrists with expertise in Lyme who are knowledgeable about the different treatment options for Lyme-induced hyperacusis.
Individual nutrient deficiencies can be determined by testing at functional medicine laboratories, ie. Metametrix ION test. There is no drug specifically designed for hyperacusis, and it can be highly frustrating to find one that helps. Any medications used for this condition are considered experimental, and as with any other treatment results vary. The following medications, which are organized by type, are listed here to aid in discussion with your personal physician. It is important to note that if a medication in a category does not work, this does not rule out other medications in the same category.
Gabapentin (Neurontin), Carbamazepine (Tegretol), Tiagabine (Gabitril), Divalproex (Depakote), Topiramate (Topamax). See Anti-Convulsants ; See Nutrient Depletion
Amitriptyline (Elavil), Clomipramine (Anafranil), Doxepin HCL (Sinequan). See TCAs
Zolmitriptan (Zomig), Rizatriptan (Maxalt), Sumatriptan (Imitrex). See SRAs
Clonazepam (Klonopin), Lorazepam (Ativan), Diazepam (Valium), Alprazolam (Xanax). See Benzodiazepines
Antivert (Meclizine). See Meclizine
NUTRIENTS and HERBS:
Lemon Bioflavonoid, Magnesium, B Vitamins (ie. B1, B6, complex), Vitamin A, Zinc, NAC, Gingko, Vinpocetine
Thiamin Deficiency and Lyme
Tinnitus Treatment Options
Drugs for Tinnitus
More on TRT
Noise Sensitivity and Magnesium
rTMS and tDCS for tinnitus
Tinnitus Treatment List
Bose noise cancellation headphones
Pink Noise CD
Arches Tinnitus Relief Formula
Tinnitus and Hyperacusis Center
Oregon Tinnitus & Hyperacusis Center
Carbamazepine in Lyme Hyperacusis
Audiologic manifestations of patients with Lyme disease
Lyme Disease and Cognitive Impairments
LymeInfo: Neuropsychiatric Lyme disease
Hyperacusis and 5-HT dysfunction
List of Ototoxins
Additional "Audiology Online" Articles
Hearing Beyond the Ears
Hyperacusis General Info
Migraine Associated Vertigo
Tinnitus (and Hyperacusis) FAQ
Intro to Central Pain Syndrome
Tri Katrina Tangin mukaan borrelia-bakteeri huijaa monia lääkäreitä sillä sen aiheuttamat oireet ovat samanlaiset kuin monissa muissa tunnetuissa taudeissa.
ALDAn tekemän tutkimuksen mukaan esim. suuri osa kroonista väsymysoireyhtymää sairastavista sairastaa Borrelioosia. Eräässä tutkimusessa selvitettiin 31:n CFS potilaan oireiden syytä. 29:llä todettiin Borrelioosi.
Amerikan psykiatrien liiton entinen puheenjohtaja, tri Paul Fink, kertoo borrelia-bakteerin kykenevän aiheuttamaan jokaisen tunnetun psykiatrisen oireiston, esim. epäsosiaalinen käytös, paniikkikohtaukset, tarkkaavaisuushäiriöt, anorexia, autismi, Asperger jne. Borrelia-bakteerin osuus oireisiin jätetään kuitenkin useimmiten huomioimatta. Allolevassa listassa on esitetty tutkimuksissa esiintulleita virhediagnooseja.
300 Medical Conditions Related to Lyme Borreliosis
Questions? Comments? Write: National Lyme Report Editor Derek Clontz. He reads and answers all e-mails, usually within minutes and always within one business day.
A Disease Frequently Misdiagnosed
Katrina Tang, M.D., HMD, founder and Director of Research at the Sierra Integrative Medicine Clinic in Reno, Nevada, states that Lyme disease eludes many doctors because of its ability to mimic many other diseases.
According to an informal study conducted by the American Lyme disease Alliance (ALDA),most patients diagnosed with Chronic Fatigue Syndrome (CFS) are actually suffering from Lyme disease. In a study of 31 patients diagnosed with CFS, 28 patients, or 90.3%, were found to be ill as a result of Lyme.
Dr. Paul Fink, past president of the American Psychiatric Association, has acknowledged that Lyme disease can contribute to every psychiatric disorder in the Diagnostic Symptoms Manual IV (DSM-IV). This manual is used to diagnose psychiatric conditions such as attention deficit disorder (ADD), antisocial personality, panic attacks, anorexia nervosa, autism and Aspergers syndrome (a form of autism) to name a few.
List of Conditions
Lyme Borreliosis causes, mimics, is manifested as, is misdiagnosed as or is a contributing factor to many conditions. The following list of over 300 conditions was compiled by means of a non exhaustive search of published scientific literature and includes:
Acrodermatitis chronica atrophicans (ACA)
Acute Acral Ischemia
Acute conduction disorders
Acute coronary syndrome
Acute exogenous psychosis
Acute peripheral facial palsy
Acute pyogenic arthritis
Acute reversible diffuse conduction system disease
Acute transitory auriculoventricular block
Acute transverse myelitis
Acute urinary retention
Acquired Immune Deficiency Syndrome (AIDS)
Amyotrophic lateral sclerosis (ALS - Lou Gehrig's Disease)
Asymmetrical hearing loss
Atraumatic spontaneous hemarthrosis
Attention Deficit Disorder (ADD)
Attention Deficit Hyperactivity Disorder (ADHD)
Benign cutaneous lymphocytoma
Benign lymphocytic infiltration (Jessner-Kanof)
Bilateral carpal tunnel syndrome
Bilateral facial nerve palsy
Bilateral follicular conjunctivitis
Brown recluse spider bite
Carpal tunnel syndrome
Cauda equina syndrome
Central vestibular syndrome
Cervical facet syndrome
Chiasmal optic neuritis
Chronic Fatigue Syndrome
Chronic muscle weakness
Complete flaccid paraplegia
Complex Regional Pain Syndrome (CRPS)
Conus medullaris syndrome
Cutaneous B-cell lymphoma
Endogenous paranoid-hallucinatory syndrome
Eosinophilic fasciitis (Shulman syndrome)
Erythema chronicum migrans
Exanthema (local and generalized)
Fatal adult respiratory distress syndrome
Focal nodular myositis
Generalised motor neuron disease
Giant cell arteritis
HLA-B27 negative sacroiliitis
Human necrotizing splenitis
Idiopathic atrophoderma of Pasini and Pierini (IAPP)
Idiopathic facial paralysis
Impaired Brainstem response
Infantile sclero-atrophic lichen
Infiltrating lymphadenosis benigna cutis
Inflammatory cerebrospinal fluid syndrome
Interstitial granulomatous dermatitis
Intracranial mass lesions
Intrauterine growth retardation
Irritable Bowel Syndrome
Isolated acute myocarditis
Isolated neuritis of the sciatic nerve
Isolated oculomotor nerve paralysis
Isolated posterior cord syndrome
Juvenile Rheumatoid Arthritis
Left sided sudden hemiparesis
Lymphadenosis benigna cutis
Morgagni-Adams-Stokes syndrome (MAS)
Morning glory syndrome
Motor neuron syndrome
Myofascial pain syndrome
Neonatal respiratory distress
Normal-pressure hydrocephalus (NPH)
Optic disk edema
Organic mood syndrome
Optic nerve lesion
Paralysis of abdominal muscles
Pars plana vitrectopy
Parsonage and Turner syndrome
Peripheral facial palsy
Peripheral vascular disorder
Persistent atrioventricular block
Polysymptomatic autoimmune disorder
Primary lymphoma of the nervous system
Progressive cerebral infarction
Progressive facial hemiatrophy (Parry-Romberg syndrome)
Progressive supranuclear paralysis
Pseudo tumor Cerebrae
Pseudoneoplastic weight loss
Ramsay Hunt syndrome (pleocytosis)
Reflex sympathetic dystrophy
Restless legs syndrome
Retinal pigment epithelium detachment
Sensorineural Hearing Loss
Seventh nerve paralysis
Sick sinus syndrome
Spontaneous brain hemorrhage
Subacute Bacterial Endocarditis
Subacute multiple-site osteomyelitis
Subacute organic psychosyndrome
Subacute multiple-site osteomyelitis
Subacute presenile dementia
Sudden infant death syndrome (SIDS)
Temporomandibular joint syndrome
Transient Ischemic Attack
Transient left ventricular dysfunction
Unilateral interstitial keratitis
Vasculitic mononeuritis multiplex
Rev Neurol (Paris). 1989;145(5):362-8.
[Neurologic forms of Lyme disease. 12 cases].
[Article in French]
Viader F, Poncelet AM, Chapon F, Thenint JP, Dupuy B, Morin P, Lechevalier B.
Service de Neurologie Dejerine, CHU de Caen.
Twelve cases of Lyme's disease with neurological complications are reported. Seven patients had meningoradiculitis of the Garin-Bujadoux-Bannwarth type, with facial palsy in 2 cases. In 1 case the radiculitis involved only the cauda equina. Two more patients had meningomyelitis. Of the remaining 3, 1 had subacute inflammatory polyneuritis with albumino-cytologic dissociation, 1 had probable dorsal epiduritis, and the last one developed parkinsonism and communicating hydrocephalus after an otherwise classical meningoradiculitis. Three patients recalled a tick bite but only one a cutaneous eruption. No arthritis or cardiac involvement were observed. In 2 cases the CSF contained pseudo-neoplastic cells. Severe pain was a prominent feature in most cases. Pain consistently and rapidly improved on high-dose intravenous penicillin, while other signs or symptoms (e.g. paresthesias or fatigue) often lasted several months. Parkinsonism and hydrocephalus were not influenced by penicillin, and both required specific therapy. Isolated neurological (both central and peripheral) involvement is not unusual in Lyme's disease and may give rise to a wide range of signs and symptoms. This diagnosis is to be considered even when other features of Borrelia burgdorferi infection are lacking.
[PubMed - indexed for MEDLINE]
Medscape Medical News from: The American Psychiatric Association's 2012 Annual Meeting
Chronic Lyme Disease Linked to ADHD in Adults
May 8, 2012 (Philadelphia, Pennsylvania) ? Chronic lyme disease (CLD) has been linked to attention-deficit hyperactivity disorder (ADHD) in adults, new research shows.
"The association between ADHD and CLD has not been identified previously," principal investigator Joel L. Young, MD, medical director, Rochester Center for Behavioral Medicine, Rochester, Minnesota, told Medscape Medical News. The survey results also corroborate earlier findings of a relationship between CLD and anxiety and depression, he said.
Dr. Young presented his research here at the American Psychiatric Association's 2012 Annual Meeting.
Participants for the survey were drawn from the 2009 Michigan Lyme Disease Association Conference. A total of 58 adults with CLD and a control group of 26 adults without CLD participated. The mean age was 48 to 49 years in both groups.
On the AD/HD Self-Report Scale (ASRS), adults with CLD endorsed more ADHD symptoms than control participants. Results were significant for both inattentive and hyperactive subunits and the combined type, Dr. Young reported.
"Cognitive deficits associated with CLD have been demonstrated before," Dr. Young said, "although this is the first survey to identify a linkage between these two conditions."
As expected, the CLD group had statistically significantly higher scores on the Fatigue Severity Scale (FSS) than the control group. The CLD group also had "dramatically higher" rates of dysthymia, generalized anxiety, major depression, and somatization.
Dr. Young said the correlation between ADHD and CLD "is novel in the research literature. Symptoms of CLD include persistent fatigue and unexplainable generalized pain. We conclude that many individuals who are diagnosed with CLD might have ADHD (inattentive type). We believe that many are diagnosed with CLD inaccurately and that ADHD symptoms might better explain their persistent pain and fatigue," he added.
Dr. Young emphasized that there is currently "little consensus about the validity of CLD. Most clinicians agree that there is a phenomenon of acute Lyme disease, but there is no consensus about whether it is a chronic condition. I believe that patients who have these symptoms often get the diagnosis of CLD because there is no other explanation for their chronic fatigue and pain."
"Many times," Dr. Young added, "the neuropsychiatric complications associated with CLD are the most problematic for individuals. My research indicates that individuals with CLD should be evaluated for ADHD. It is unclear if treating ADHD will help these individuals' symptoms of pain and fatigue."
Interpret With Caution
Commenting on the study for Medscape Medical News, Brian Fallon, MD, MPH, director of the Lyme and Tick-Borne Diseases Research Center, Columbia University, New York City, cautioned against drawing any firm conclusions from this survey. Surveys are "notorious for elevating psychiatric complaints," he said.
"Most carefully conducted neurocognitive studies have identified problems with memory, processing speed, and verbal fluency in Lyme patients ? and not attention problems. Attention problems are primarily seen in depression," added Dr. Fallon, who was not involved in the study.
Dr. Young is the author of the book ADHD Grown Up: A Guide to Adolescent and Adult ADHD (W.W. Norton, 2009). He has disclosed relationships with Cyberonics Inc, Eli Lily, Novartis, Otsuka, Pfizer, Shire, Forest, Merck, Bristol Myers Squibb Co, and Shionogi Inc. Dr. Fallon has disclosed no relevant financial relationships.
The American Psychiatric Association's 2012 Annual Meeting. Abstract NR8-30. Presented May 8, 2012.
Med Clin (Barc). 2012 May 12;138(13):591-2. Epub 2011 Nov 16.
[Abdominal pain and wall distension as the onset form of neuroborreliosis].
[Article in Spanish]
Arruti M, Fuertes A, Amato E, López de Munain A.
Servicio de Neurología, Hospital Donostia, San Sebastián, España.
[PubMed - in process]
Krooniset tulehdustaudit voivat aiheuttaa vatsan aortta-aneurysman. Tutkimuksessa havaittiin esim. borrelia-bakteerin voivan olla tautiin.
Presence of Borrelia burgdorferi sensu lato antibodies in
the serum of patients with abdominal aortic aneurysms
European Journal of Clinical Microbiology & Infectious
Diseases, Vol. 31, No. 5 (2012), 781-789.
Infectious agents are likely to play a role in the
pathogenesis of chronic inflammatory diseases, including
abdominal aortic aneurysms (AAAs). The goal of this study
was to determine if Borrelia burgdorferi sensu lato (sl), a
microorganism responsible for Lyme disease, is involved in
the etiology of AAAs.
The presence of serum antibodies against B. burgdorferi sl
was measured with enzyme-linked immunosorbent assay (ELISA)
and confirmed by Western blotting in 96 AAA and 108
peripheral artery disease (PAD) patients. Polymerase chain
reaction (PCR) was used for the detection of
Borrelia-specific DNA in the aneurysm wall.
Among AAA patients 34% and among PAD patients 16% were seropositive for B. burgdorferi sl antibodies (Fisher's exact test, p= 0.003;
odds ratio [OR] 2.79; 95% confidence interval [CI] 1.37?5.85).
In the German general population, 3?17% are seropositive for
Borrelia antibodies. No Borrelia DNA was detected in the aneurysm wall.
Our findings suggest a relationship between AAAs and B.
burgdorferi sl. We hypothesize that the underlying mechanism
for B. burgdorferi sl in AAA formation is similar to that by
the spirochete Treponema pallidum; alternatively, AAAs could
develop due to induced autoimmunity via molecular mimicry
due to similarities between some of the B. burgdorferi sl
proteins and aortic proteins.
Free, full text of this open access article is available for
download as a pdf file (200.1 KB):
http://www.springerlink.com/content/370 ... lltext.pdf
Hoito: IV keftriaksoni + suun kautta doksisykliiniä + steroideja. Toinen sai ainoastaan iv keftriaksonin. (2012)
http://www.dovepress.com/case-report-pa ... ticle-OPTH
Case report: papillitis as the sole ocular sign in Lyme disease
Authors: McVeigh K, Vakros G
Published Date July 2012 Volume 2012:6 Pages 1093 - 1097
Katherine McVeigh, Georgios Vakros
Department of Ophthalmology, Raigmore Hospital, Inverness, United Kingdom
Background: Lyme disease is a spirochetal disease responsible for a multitude of ocular and systemic manifestations, and patients may present to ophthalmologists and general clinicians with a wide variety of generalized and ocular signs which can result in chronic and disabling sequelae. Here we report two cases of patients suffering with Lyme disease who developed a rare associated papillitis.
Methods: A 48-year-old Scottish man presented with diminished visual acuity, painful ocular eye movements, photophobia, and mild ataxia. Fundus examination revealed bilateral disc swelling with associated hemorrhages in the right eye. Following exclusion of raised intracranial pressure as the cause of the findings, enzyme-linked immunosorbent assay and Western blot serology confirmed a positive result for Borrelia burgdorferi which, along with ophthalmic signs and exposure to an endemic area, confirmed the diagnosis of Lyme disease. A 79-year-old gentleman presented with intermittent short-duration ?gray film? in his left eye. Fundus examination revealed left optic disc swelling. He was positive for Lyme?s serology and his condition was treated with 2 weeks of intravenous ceftriaxone.
Results: The first patient?s inflammation resolved and visual acuity returned to normal following a course of high-dose steroids and intravenous ceftriaxone, followed by oral doxycycline. The second patient?s condition improved with high-dose intravenous ceftriaxone.
Conclusion: These patients highlight the fact that Lyme disease should be considered as a differential diagnosis for patients presenting with papillitis. With the incidence of this disease rising and more cases being reported, practitioners in Lyme-endemic areas need to be aware of the various manifestations so that appropriate referrals for treatment can be made.
Keywords: Lyme disease, ocular papillitis, Borrelia burgdorferi
Authors: Hidri N, Barraud O, de Martino S, Garnier F, Paraf F, Martin C, Sekkal S, Laskar M,
Jaulhac B, Ploy MC
Citation: Clin. Microbiol. Infect. 2012(Aug)
Location: CHU Limoges, Laboratoire de Bactériologie-Virologie-Hygiène, Limoges
Centre National de Référence des Borrelia, Laboratoire de Bactériologie des
Hôpitaux Universitaires de Strasbourg, Strasbourg CHU Limoges, Service d'Anatomie Pathologique,
Limoges Univ Limoges, EA 3842 Faculté de Médecine, Limoges CHU Limoges,
Service de Chirurgie Thoracique et Cardio-Vasculaire et Angiologie, Limoges, France.
ABSTRACT: Lyme borreliosis is a common tick-borne disease with a wide variety of clinical manifestations. Cardiac involvement has been reported during both the acute phase (atrioventricular block, pericarditis) and the chronic stage (dilated cardiomyopathy), but is rare (<5%). Here we describe the first case of Borrelia afzelii Lyme endocarditis, in a 61-year-old man living in an endemic area of France. The diagnosis was confirmed by detection of B. afzelii DNA in the mitral valve by specific real-time PCR. He was treated empirically with amoxicillin for 6 weeks and remains well 12 months later.
© 2012 The Authors. Clinical Microbiology and Infection © 2012 European Society of Clinical Microbiology and Infectious Diseases.
Authors: Littman MP
Citation: J Vet Emerg Crit Care (San Antonio) 2013(Mar)
Location: Department of Clinical Studies-Philadelphia, University
of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, 19104-6010.
OBJECTIVE: To review what is known and highlight knowledge gaps
regarding Lyme nephritis (LN).
DATA SOURCES: Publications identified via PubMed using the keywords
"Borrelia burgdorferi," "Borreliosis," "glomerulonephritis,"
"autoimmunity," and "retriever," and as
generated by investigators working in the fields of Borreliosis and
HUMAN DATA SYNTHESIS: Postborrelial immune-mediated glomerulonephritis
was described recently in 6 people; 3 responded to
antimicrobials/steroids, 1 to antimicrobials/angiotensin-converting
enzyme inhibitor/warfarin, 1 required hemodialysis but became
hemodialysis independent after 5 months and treatment with
antimicrobials, steroids, plasmapheresis, immunoglobulin, and 1 did not
respond to steroids and angiotensin-converting enzyme inhibitor and
still requires hemodialysis.
VETERINARY DATA SYNTHESIS: Lyme nephritis is seen in <1-2% of Lyme
seropositive dogs, with an average onset at 5-6 years. Labrador and
Golden Retrievers are predisposed to this condition. Prior or concurrent
lameness is described in 9-28% cases. Historical presentations include
acute progressive protein-losing nephropathy with membranoproliferative
glomerulonephritis, tubular necrosis/regeneration, and interstitial
nephritis, but possibly milder forms exist. Complications include
thromboembolic events, hypertension, effusive disease, and
oliguric/anuric renal failure. Diagnostic tests help stage disease and
rule out other causes. Renal biopsy is advocated early, when
intervention may help, and to prove if immune-complex disease exists.
Treatment includes standard therapy for protein-losing nephropathy,
long-term antimicrobials, and perhaps immunosuppressive therapy.
CONCLUSIONS: There is no experimental model of LN to study predisposing
factors, pathogenesis, onset, progression, treatment, or prevention.
There are no predictive tests to identify the few individuals at highest
risk, therefore all seropositive dogs should be screened and monitored
for proteinuria. Lyme
nephritis mimics other forms of protein-losing
nephropathy and sometimes Leptospirosis. Renal biopsy helps show if
immune-complex disease exists, but may not prove LN specifically. More
studies are warranted on dogs with Lyme-specific immune-complex
deposition to evaluate risk factors, understand pathogenesis,
variability of expression, and to validate treatment and prevention
© Veterinary Emergency and Critical Care Society 2013.
Wednesday, April 10, 2013
Peripheral neuropathy: a very common Lyme problem
In my practice, one of the most common set of symptoms, or a syndrome relate to peripheral neuropathy. Peripheral neuropathy is caused by nerve damage, which may be temporary, stable, progressive, mildly bothersome or disabling: Nerves are comprized of two parts which may be damaged: 1) axons, the body of the nerve and 2) myelin, the sheath around the axons of nerves. Nerves are then divided into sensory neurons ( associated with sensation) and motor neurons( associated with muscle activity). The nerves can come from different pathways: spinal nerve roots, the dorsal ganglia, peripheral nerve trunks and branches, autonomic nerves. Neuropathies can effect sensory nerves, motor nerves or more commonly both.
Differences between axonal and demylinating neuropathy can be seen with a routine exam: large sensory fibers abnormalities may be associated with decreased sensation to pin prick, light touch and vibration. All that is needed is something sharp and a tuning fork. Small, unmylinated sensory fiber abnormalities associated with decreased temperature sensation.
Sensory symptoms of axonal small fiber neuropathy, may for exmple, inclde: burning pain, radiating/lancinating/ electrical like sensations, pins and needles, increased sensation to light touch, numbness and reduced sensation.
Motor symptoms may include: weakness, muscle wasting, cramps, fasiculations, difficulty climbing stairs, decreased hand grip and restless leg syndrome.
Major characteristics of axonal vs demylelinating neurve damage can be seen with the EMG/NCV. Simply put: Axonal problems are seen with needle portion of the test and demyelinating problems are seen with the shocking part of the exam.
Some patients, with clear symptoms and abnormal physical examinations have negative EMGs. There is another test.
Patients may have small-fiber neuropathy not visable on an EMG. This can be diagnosed with a biopsy of 2-3 areas of skin sent to a specialty lab.
The lab reports the "ENFD" - Epidermal Nerve Fiber Density. The test is fairly accurate.( I can perform this simple test in my office).
Most treatments for neuropathy are only symptomatic. The only therapy I have found to be curative is IViG. This therapy is extraordinarily expensive, costing $10,000 per dose given every 3-4 weeks. The FDA has approved IViGfor a limited number of conditions. It may be possible to get insurance coverage for some forms of neuropathy like CIDP which is discussed elswhere.
Korvalehden ihomuutos, erythema, on joko borreliabakteerin aiheuttama lymfosytooma tai borreliabakteerin aiheuttama paikallinen ihomuutos. Tutkimuksen taapsuselostuksessa borreliabakteeri aiheutti korvalehden rustotulehduksen eli kondriitin. Yleisemmin kondriitilla tarkoitetaan rustotulehdusta lapaluiden seudulla ns rutiseva lapaluu. Potilaan oireet hävisivät keftriaksonihoidolla.
Erythema of the ear lobe in the context of Lyme disease is caused by either borrelial lymphocytoma or localized erythema migrans. Here we present a case of chondritis limited to the ear cartilage caused by Lyme disease. The patient was treated with ceftriaxone with complete resolution of symptoms.
Startle Myoclonus Induced by Lyme Neuroborreliosis
Julia Schoof, Christian Kluge, Hans-Jochen Heinze, Imke Galazky
J Med Case Reports. 2013;7(124)
Introduction: The normal startle response is a form of physiological myoclonus. Its anatomic origin is probably the brain stem. Pathologic startles are defined as reproducible exaggerated startle responses to trivial and not surprising stimuli. Symptomatic forms of an exaggerated startle response can be due to a variety of brain stem disorders. We have, however, found scant data about an exaggerated startle reflex induced by Lyme neuroborreliosis. We therefore report the case of a patient with this unusual presentation.
Case presentation: A 69-year old Caucasian man presented with a two-week history of a pronounced startle myoclonus, as well as a four-week history of double vision, gait disturbance and severe lancinating pain in his upper thoracic region. Neurological examination showed an excessive startle reaction of his upper trunk evoked by visual and tactile stimulation, a positive sign of Lhermitte, mild right-sided palsy of his sixth and seventh cranial nerve, moderate dysarthria, very brisk deep tendon reflexes, pallhypesthesia of his legs, and an atactic gait disturbance. A diagnosis of a Lyme neuroborreliosis was confirmed by cerebrospinal fluid examination. Under intravenous treatment with ceftriaxone, our patient improved considerably with complete remission in a follow-up at two months.
Conclusions: This case illustrates the chameleon role that neuroborreliosis likes to play: although the wide spectrum of different symptoms that neuroborreliosis can present with has been described, to the best of our knowledge this is the first case report about a symptomatic form of a pathologic startle response as the predominating sign of Lyme neuroborreliosis.
• Väsymys, uupumus
• Paikkaa vaihtavat lihas- tai nivelkivut, jäsensäryt, kuin ”flunssa” ilman nuhaa, yskää tai kurkkukipua
Muut tuki –ja liikuntaelinoireet
• Niveltulehdus eli artriitti: synoviitti ja hydrops (harvoin)
• Jännetuppitulehdus (tendiniitti, daktyliitti) ja luutulehdus (harvoin)
Ääreishermoston oireet ja meningiitti
• Facialis-, abducens-, oculomotoriuspareesi, tinnitus
• Polttavat kivut, tuntomuutokset, kävelyvaikeudet, raajahalvaukset, rakon tai sulkijalihaksen toiminnanhäiriöt. Huom lihas-, nivel- ja joskus rinta- ja vatsakivut (meningoradikuliitti, Bannwarthin syndrooma)
• Plexusneuriitti, mononeuritis multiplex
• Lymfosytäärinen meningiitti (voi olla toistuvia episodeja, ei välttämättä niskajäykkyyttä)
• Muistihäiriöt, kognition häiriöt (potilas huomaa), sekavuus, persoonallisuusmuutos (ympäristö huomaa)
• Pikkuaivoataksia, myoclonus, apraksia, hemipareesi, Parkinson-oireet
• Akuutti halvausoireisto (vaskuliitti)
• Rytmihäiriötuntemukset (tarv. EKG, holter, ECHO)
• Perikardiitti, myokardiitti, eteiskammiokatkos, sydämen vajaatoiminta
• Diplopia, kaksoiskuvat (aivohermotulehdukseen viittaava oire)
• Silmien punoitus
• Silmän takainen kipu (voi liittyä meningiittiin)
• Diagnosoitu silmän sidekalvon, värikalvon, näköhermon tai verkkokalvon tulehdus
• Lymfosytooma, paikallinen disseminaatio
– tummanpunainen pahkura puremapaikan lähellä, esim korvanlehdessä tai nännipihassa
Endocrine Abstracts (2010) 22 P188
Case report of Borrelia burgdorferi infection as a possible trigger of Riedel’s thyroiditis
Gábor László Kovács, István Szabolcs, Zoltán Görömbey, László Kovács, Erika Hubina, Judit Dénes & Miklós Góth
Background: The detectable levels of thyroid antibodies in patients suffering from Riedel’s chronic fibrosing thyroiditis (RT) suggest a link between RT and Hashimoto’s thyroiditis, but the pathogenesis of RT is not really known. Lyme disease is the most frequent tick-borne infection with variable manifestations in different organs caused by Borrelia burgdorferi (Bb).
Case report: A 59-year-old woman presented in our outpatient clinic with a painful swelling and cervical discomfort in the anterior area of the neck. 30 years ago she was treated with thiamazol for Graves’ disease. The symptoms started following two tick bites on the neck. She presented with elevated inflammatory markers (westergren 91 mm/h, CRP 88.6 mg/l), anaemia, and thrombocytosis (haemoglobin 112 g/l, PLT 513 G/l) with normal level of procalcitonin and white blood cells. Primary hypothyroidism was detected (TSH 37.8 μIU/ml, fT4 6.22 pmol/l). Ultrasonography showed bilateral enlargement, hypovascularisation of the thyroid with multiple hypoechogenic nodular formation and bilateral large lymph nodes. Tc scintigraphy showed a low Tc uptake (0.69%). Transitional methylprednisolone treatment with thyroxin substitution was started. The planned near total thyroidectomy was unsuccessful. The histological investigation suggested the diagnosis of RT. The microbiological tests confirmed a Bb acute infection with elevated IgM/IgG levels. Amoxicillin treatment (3×500 mg/21 days) was advised, then pulsatile steroid therapy administered (250 mg methylprednisolone/7 day cycles up to 1500 mg). After treatment the symptoms and inflammatory laboratory results improved; the former trachea compression did not worsen. According to the literature data some parts of the human TSH receptor match outer surface protein A, flagellar rotation protein A, DNA recombinase/ATP dependent helicase of Bb.
Conclusion: Our case strengthens the former hypothesis: Bb might be an environmental trigger of autoimmune thyroid disease through a molecular mimicry mechanism. To our knowledge this is the first case of Bb infection and Riedel’s thyroiditis co-morbidity.
SENSORINEURAL HEARING LOSS: A COMPLEX FEATURE IN LYME DISEASE.
Authors: Bertholon P
Citation: Otol. Neurotol. 2013(Sep)
Location: Department of Otorhinolaryngology, Saint Etienne, France.
No abstract is included.
Damage of collagen and elastic fibres by borrelia burgdorferi - known and new clinical and histopathological aspects.
Authors: Müller KE
Citation: Open Neurol J 2012; 6: 179-86.
Location: Medical Practice for Dermatology, Venerology, Occupational Dermatology and Environmental Medicine, Kempten, Bavaria, Germany.
Lyme Borreliosis, or Lyme's disease, manifests itself in numerous skin conditions. Therapeutic intervention should be initiated as soon as a clinical diagnosis of erythema migrans is made. The histopathology of some of the skin conditions associated with Lyme Borreliosis is characterised by structural changes to collagen, and sometimes also elastic fibres. These conditions include morphea, lichen sclerosus et atrophicus and acrodermatitis chronica atrophicans. More recently, further skin conditions have been identified by the new microscopic investigation technique of focus floating microscopy: granuloma annulare, necrobiosis lipoidica, necrobiotic xanthogranuloma, erythema annulare centrifugum, interstitial granulomatous dermatitis, cutaneous sarcoidosis and lymphocytic infiltration; these conditions also sometimes cause changes in the connective tissue.
In the case of ligaments and tendons, collagen and elastic fibres predominate structurally. They are also the structures that are targeted by Borrelia. The resultant functional disorders have previously only rarely been associated with Borreliosis in clinical practice. Ligamentopathies and tendinopathies, spontaneous ruptures of tendons after slight strain, dislocation of vertebrae and an accumulation of prolapsed intervertebral discs as well as ossification of tendon insertions can be viewed in this light.
Ruotsalaistutkimus: Punkin purema voi laukaista liha-allergian
Ruotsalaistutkimuksen mukaan punkin purema voi laukaista allergian punaiselle lihalle. Tukholman Södersjukhusetissa on tunnistettu 50 tapausta, jossa potilas on saanut liha-allergian punkin pureman seurauksena. Oireet vaihtelevat nokkosihottumasta anafylaksiaan eli äkilliseen, hengenvaaralliseen allergiseen reaktioon. Suomalaistutkija pitää tietoa yllättävänä, mutta ei mahdottomana.
Punkki Kuva: YLE
Punkin puremat voivat aiheuttaa borrelioosia ja puutiaisaivokuumetta. Tuoreen ruotsalaistutkimuksen mukaan ne voivat myös laukaista allergian punaiselle lihalle.
– Kuulostaa todella yllättävältä, punkkitutkija Antti Vaheri Helsingin yliopistosta sanoo. Hän ei kuitenkaan pidä tietoa mahdottomana.
Ruotsalaistutkimuksen mukaan potilaat ovat saaneet punaisen lilhan syömisestä allergiareaktioita nokkosihottumasta anafylaksiaan, äkilliseen, hengenvaaralliseen allergiseen reaktioon. Potilaiden kasvot ovat punehtuneet ja turvonneet. Lisäksi heillä on ollut vatsaoireita, kuten pahoinvointia, ripulia ja vatsakipuja.
– Meillä on 50 potilasta, joilla olemme todenneet liha-allergian punkin pureman jälkeen, ylilääkäri ja allergologian erityislääkäri Maria Starkhammar Tukholman Södersjukhusetista sanoo sanomalehti Dagens Nyheterissä.
"Yhteys on voimakas"
Lähes puolet on saanut anafylaksian, äkillisen ja hengenvaarallisen allergisen reaktion, joka aiheuttaa hengenahdistusta ja verenpaineen laskua. Tutkijoiden mukaan he ovat pystyneet todistamaan liha-allergian yhteyden punkin puremaan.
– Yhteys on hyvin voimakas ja uskon, että löydämme lisää tapauksia, kliinisen immunologian professori Marianne van Hage Solnan Karoliinisesta instituutista sanoo.
Ruotsalaistutkijoiden mukaan punkkien vatsasuolistokanavassa on entsyymi alfa-galaktosidaasia. Sitä on nelijalkaisissa nisäkkäissä, mutta ei ihmisissä tai apinoissa, ja tutkijat ovat todentaneet sen yhteyden liha-allergiaan.
Suomalaistutkija uskoo, että entsyymiä voi olla punkin syljessä.
– Punkin sylki, joka on ainoa, mikä punkin puremassa siirtyy. Se on kuin apteekki. Siellä on ties mitä, mitä punkki on miljoonien vuosien kehityksen aikana kehittänyt, punkkitutkija Antti Vaheri sanoo.
– On täysin mahdollista, että siellä on tällainen galaktosidaasi, hän toteaa.
Ruotsalaistutkijat löysivät ensimmäiset tapaukset vuonna 2009. Heidän mukaansa potilaat ovat kehittäneet allergian punaiselle lihalle, kuten naudan-, sian- ja lampaanlihalle.
DN: Svensk studie ger svar på allergigåta
http://www.dn.se/nyheter/vetenskap/sven ... lergigata/
Svensk studie ger svar på allergigåta
Publicerad 2013-09-26 06:00
Fästingbett kan ligga bakom allvarlig allergi mot rött kött. Det visar en ny svensk studie.
– Vi upptäckte tre fall 2009. Nu har vi nästan 50 patienter där vi konstaterat köttallergi som är kopplad till fästingbett, säger Maria Starkhammar, överläkare och specialist i allergologi vid Södersjukhuset.
Fästingar orsakar inte bara borrelia och tbe. En ny svensk studie visar att fästingbett också kan trigga utbrott av köttallergi, en ovanlig form av födoämnesallergi. Nästan samtliga patienter som kommit till Södersjukhuset har fått nässelutslag av att äta rött kött – exempelvis nöt, fläsk- och lammkött – men många får också rodnad och svullnad i ansiktet samt magsymtom som illamående, diarré och buksmärtor.
Nästan hälften av patienterna har också drabbats av den svåraste formen av allergisk reaktion – anafylaxi. Den kännetecknas av andningspåverkan och blodtrycksfall.
Mia Lindström är en av Maria Starkhammars patienter där man såg sambandet mellan fästingbett och utbrott av köttallergi.
– Jag åt köttfärssås och fick en kraftig allergisk reaktion cirka sex timmar senare. Det var första steget för att upptäcka att jag var allergisk mot kött. Jag hade haft känningar tidigare men ingen så kraftig reaktion, säger Mia Lindström.
Och kopplingen till fästingbett är tydlig.
– Jag är den enda i familjen som får fästingbett och har fått flera. Jag prövade att äta älggryta men tålde inte heller det.
I dag äter hon inte alls rött kött.
– Man blir expert på alternativ. Det blir mycket kyckling och en del fisk, säger Mia Lindström.
Diagnosen köttallergi är svår att ställa.
– Problemet är att ofta misstänker varken patient eller läkare att det rör sig om köttallergi. Kött är något man har ätit i hela sitt liv och förutom att man inte får symtomen varje gång man äter kött så är reaktionen till skillnad från andra allergiska reaktioner fördröjd, säger Maria Starkhammar.
Marianne van Hage, professor i klinisk immunologi vid Karolinska institutet och överläkare vid Karolinska universitetssjukhuset, har genomfört de kliniska testerna som lett fram till att man kunnat se sambandet.
– Vi har kunnat visa att kolhydraten alpha-gal finns i fästingens magtarmkanal. Denna upptäckt har gjort att vi nu med säkerhet kan säga att det finns en koppling mellan fästingbett och köttallergi.
– Vid fästingbett finns det risk att utveckla allergiantikroppar mot alpha-gal. Alpha-gal finns förenklat hos fyrfota däggdjur men inte hos människor och apor, säger Marianne van Hage.
Samtliga av de nästan 50 patienter som Maria Starkhammar och Marianne van Hage har diagnostiserat som köttallergiker är fästingbitna.
– Sambandet är mycket starkt och jag tror att vi definitivt kommer att hitta fler. Det finns ett mörkertal av människor som har oförklarliga besvär och där förklaringen kan vara denna, säger Marianne van Hage.
Rev Med Interne. 2010 Jan 13; [Epub ahead of print]
[Recurrent nerve palsy due to Lyme disease: Report of two cases.]
[Article in French]
Martzolff L, Bouhala M, Dukic R, Saraceni O, Wilhelm JM, Bombaron P, Kieffer P.
Service de medecine interne et endocrinologie, hopital Emile-Muller, 87, avenue
d'Altkirch, BP 1070, Mulhouse cedex, France.
INTRODUCTION: Neuroborreliosis can be a difficult diagnosis which requires
epidemiologic, clinical and biologic arguments. CASE REPORTS: We report two
patients who presented with a recurrent laryngeal nerve palsy with positive Lyme
serology and favorable outcome after antibiotic therapy. In one case, a
lymphocytic meningitis with intrathecal production of specific antibodies was
evidenced. CONCLUSION: Recurrent laryngeal nerve palsy is an uncommon
manifestation of neuroborreliosis. Lyme serology is an important tool when
neurologic disorder occurs because of an atypical course of Lyme disease.
Copyright (c) 2009 Societe nationale francaise de medecine interne (SNFMI).
Published by Elsevier SAS. All rights reserved.
http://eutils.ncbi.nlm.nih.gov/entrez/e ... md=prlinks
PMID: 20079561 [PubMed - as supplied by publisher]
the Neurological Sciences
Lyme optic neuritis
Frédéric Blanc, et al
Lyme optic neuritis (ON) is a rare disease and only a few cases have been reported. We describe two cases of isolated Lyme ON, one with recurrence 9 months after the appearance of initial symptoms. Diagnosis criteria for multiple sclerosis and neuromyelitis optica were not met. The etiological diagnosis was based on European case definition criteria for neuroborreliosis. Both patients had positive serum and cerebrospinal fluid serology, a positive intrathecal anti-Borrelia antibody index, and a good outcome on ceftriaxone. Specific diagnosis of Lyme ON is important since improvement of visual acuity is possible with specific antibiotherapy, even after many months.
Taudinkuvaan kuuluu paitsi symmetrinen lihasheikkous hartia- ja lantioseudussa myös varsinkin käsien mutta kenties kasvojenkin tummanpunaisia ihottumaläiskiä. Lihasheikkous ja väsymys ovat taudin oireita. Noin kolmasosalla sairastuneista on myös nielemisongelmia. Taustalla saattaa olla toisinaan muita sairauksia. (lihastautiliitto)
Keuhkofibroosissa keuhkokudos korvautuu vähitellen sidekudoksella. Tämä aiheuttaa ärsytystä, mikä ilmenee pitkäaikaisena, kuivana yskänä. Sidekudoksen seurauksena keuhkojen kyky hapettaa verta heikkenee, mikä ilmenee hiljalleen pahenevana hengenahdistuksena. Aluksi ahdistus tuntuu epätavallisena hengästymisenä ruumiillisessa rasituksessa. (Terveyskirjasto)
Acute Lyme infection presenting with amyopathic dermatomyositis and rapidly
fatal interstitial pulmonary fibrosis:a case report
Nguyen H, Le C, Nguyen H.
Journal of Medical Case Reports 2010, 4:187. Published online June 21, 2010.
Dermatomyositis has been described in the setting of lyme infection in
only nine previous case reports. Although lyme disease is known to
induce typical clinical findings that are observed in various collagen
vascular diseases, to our knowledge, we believe that our case is the
first presentation of acute lyme disease associated with amyopathic
dermatomyositis, which was then followed by severe and fatal
interstitial pulmonary fibrosis only two months later.
We present a case of a 64-year-old African-American man with multiple
medical problems who was diagnosed with acute lyme infection after
presenting with the pathognomonic rash and confirmatory serology. In
spite of appropriate antimicrobial therapy for lyme infection, he
developed unexpected amyopathic dermatomyositis and then interstitial
This case illustrates a potential for Lyme disease to produce clinical
syndromes that may be indistinguishable from primary connective tissue
diseases. An atypical and sequential presentation (dermatomyositis and
interstitial lung disease) of a common disease (Lyme infection) is
discussed. This case illustrates that in patients who are diagnosed with
lyme infection who subsequently develop atypical muscular, respiratory
or other systemic complaints, the possibility of severe rheumatological
and pulmonary complications should be considered.
Free, full text of this open access article as a provisional .pdf file:
http://www.jmedicalcasereports.com/cont ... -4-187.pdf
http://www.wemjournal.org/article/S1080 ... 7/abstract
Appalachian Trail Hikers’ Ability to Recognize Lyme Disease by Visual Stimulus Photographs
Judith M. Knoll, DOemail address
Andrea C. Ridgeway, DO, MPH
Christine M. Boogaerts, DO
Glenn A. Burket III
published online 15 January 2014.
Lyme disease is the most common vector-borne infectious disease in North America. With nearly 2,500 Appalachian Trail (AT) hikers entering the endemic area for as long as 6 months, exposure to the disease is likely. The characteristic exanthem of erythema migrans (EM) should be a trigger for seeking medical treatment, and its recognition in this relatively isolated environment is important.
The purpose of this study was to determine the ability of AT hikers to identify EM, the exanthem of Lyme disease.
Hikers were administered a photographic stimulus in this Internal Review Board–approved pilot study. Historical hiking data, basic demographics, and self-reported treatment and diagnosis were collected.
In all, 379 responses were collected by 4 researchers at 3 geographically separate locations at or proximate to the AT from June 2011 to May 2012. Fifty-four percent of respondents (206 of 379) were able to recognize the photographs of EM/Lyme disease; 46% could not. Of those who did recognize EM, 23 (6%) had seen it either on themselves or on another hiker while on the AT. A total of 37 hikers stated that they had been diagnosed with Lyme disease while hiking, and of these, 89% were treated with antibiotics. Thirteen of these 37 hikers (35%) diagnosed with Lyme disease had visualized an embedded tick. Nine percent of all respondents reported they had been diagnosed with Lyme disease by a healthcare practitioner, whether from EM, symptomatology, or by titer.
This study suggests that hikers are poorly able to recognize the characteristic exanthem of Lyme disease but have a high exposure risk.
Key words: Appalachian Trail, hikers, erythema migrans, recognition of exanthem, photographic stimulus, Lyme disease
Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria
Correspondence: Judith Miklossy email@example.com
International Alzheimer Research Center, Prevention Alzheimer Foundation, Martigny-Combe, Switzerland
Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90
The electronic version of this article is the complete one and can be found online at:http://www.jneuroinflammation.com/content/8/1/90
© 2011 Miklossy; licensee BioMed Central Ltd
It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 × 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases.
Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro by exposure of mammalian cells to spirochetes. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research.
Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.
Alzheimer's disease; bacteria; Borrelia burgdorferi; dementia; infection; Lyme disease; periodontal pathogen; spirochetes; Treponema; syphilis
The recognition that pathogens can produce slowly progressive chronic diseases has resulted in a new concept of infectious diseases. The pioneering work of Marshall and Warren has established that Helicobacter pylori (H. pylori) causes stomach ulcer . Also the etiologic agent of Whipple's disease was revealed to be another bacterium, Tropheryma whippeli. Recent reports have documented that infectious agents also occur in atherosclerosis, cardio- and cerebrovascular disorders [2-10], diabetes mellitus [11-16], chronic lung [17-20] and inflammatory bowel diseases[1,21-25], and various neurological and neuropsychiatric disorders [26-31].
Nearly a century ago, Fischer, Alzheimer and their colleagues [32,33] discussed the possibility that microorganisms may play a role in the formation of senile plaques. Historic data indicate that the clinical and pathological hallmarks of syphilitic dementia in the atrophic form of general paresis, caused by chronic spirochetal infection, are similar to those of AD. There is an increasing amount of data that indicates that spirochetes are involved in the pathogenesis of AD. This review presents historic and new data related to the involvement of spirochetes in AD. The goal was to critically analyze the association and causality between spirochetes and AD, based on the substantial amount of data available and on established criteria of Koch [34,35] and Hill 
More at website: http://www.jneuroinflammation.com/content/8/1/90
http://benthamscience.com/open/toneuj/a ... TONEUJ.pdf
Published online Dec 31, 2012. doi: 10.2174/1874205X01206010179
Damage of Collagen and Elastic Fibres by Borrelia Burgdorferi – Known and New Clinical and Histopathological Aspects
Kurt E Müller*
Author information ► Article notes ► Copyright and License information ►
Lyme Borreliosis, or Lyme’s disease, manifests itself in numerous skin conditions. Therapeutic intervention should be initiated as soon as a clinical diagnosis of erythema migrans is made.
The histopathology of some of the skin conditions associated with Lyme Borreliosis is characterised by structural changes to collagen, and sometimes also elastic fibres. These conditions include morphea, lichen sclerosus et atrophicus and acrodermatitis chronica atrophicans.
More recently, further skin conditions have been identified by the new microscopic investigation technique of focus floating microscopy: granuloma annulare, necrobiosis lipoidica, necrobiotic xanthogranuloma, erythema annulare centrifugum, interstitial granulomatous dermatitis, cutaneous sarcoidosis and lymphocytic infiltration; these conditions also sometimes cause changes in the connective tissue. In the case of ligaments and tendons, collagen and elastic fibres predominate structurally. They are also the structures that are targeted by Borrelia. The resultant functional disorders have previously only rarely been associated with Borreliosis in clinical practice. Ligamentopathies and tendinopathies, spontaneous ruptures of tendons after slight strain, dislocation of vertebrae and an accumulation of prolapsed intervertebral discs as well as ossification of tendon insertions can be viewed in this light.
Keywords: Lyme Borreliosis, collagen fibres, elastic fibres, skin, connective tissue, tendons, ligaments, diverticulum.
J Clin Invest. Jan 2, 2014; 124(1): 311–320.
Published online Dec 16, 2013. doi: 10.1172/JCI72339
Lysosomal β-glucuronidase regulates Lyme and rheumatoid arthritis severity
Kenneth K.C. Bramwell,1 Ying Ma,1 John H. Weis,1 Xinjian Chen,1 James F. Zachary,2 Cory Teuscher,3 and Janis J. Weis1
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most prevalent arthropod-borne illness in the United States and remains a clinical and social challenge. The spectrum of disease severity among infected patients suggests that host genetics contribute to pathogenic outcomes, particularly in patients who develop arthritis. Using a forward genetics approach, we identified the lysosomal enzyme β-glucuronidase (GUSB), a member of a large family of coregulated lysosomal enzymes, as a key regulator of Lyme-associated arthritis severity. Severely arthritic C3H mice possessed a naturally occurring hypomorphic allele, Gusbh. C57BL/6 mice congenic for the C3H Gusb allele were prone to increased Lyme-associated arthritis severity. Radiation chimera experiments revealed that resident joint cells drive arthritis susceptibility. C3H mice expressing WT Gusb as a transgene were protected from severe Lyme arthritis. Importantly, the Gusbh allele also exacerbated disease in a serum transfer model of rheumatoid arthritis. A known GUSB function is the prevention of lysosomal accumulation of glycosaminoglycans (GAGs). Development of Lyme and rheumatoid arthritis in Gusbh-expressing mice was associated with heightened accumulation of GAGs in joint tissue. We propose that GUSB modulates arthritis pathogenesis by preventing accumulation of proinflammatory GAGs within inflamed joint tissue, a trait that may be shared by other lysosomal exoglycosidases.
"What we find too often is that when a patient has symptoms that a diagnosis has not been made for, mitochondrial disorders often get invoked as a diagnosis. We frequently see patients labeled with a mitochondrial disease diagnosis who in fact have something else, whether it be a genetic syndrome, or another medical issue like celiac or Lyme disease."
Understanding Mitochondrial Disorders - Sumit Parikh MD
Online Health Chat with Sumit Parikh, MD
January 14, 2010 | Reviewed on January 28, 2014 by Sumit Parikh, MD
Cleveland_Clinic_Host: Mitochondrial disorders can affect organs, motor function and the nervous system. Individuals experience a wide array of symptoms and degrees of severity. Although commonly seen in infants and children this chronic and genetic disease can develop at any age. Diagnosis of this disease can be difficult. Cleveland Clinic Pediatric Neurology is ranked in the top 4 in the country with many of its physicians specializing in the research and treatment of mitochondrial disease.
Mitochondria are tiny organelles found in almost every cell in the body. These organelles are responsible for creating 90% of cellular energy necessary to maintain life and support growth. Mitochondrial disease is when mitochondria in the cells fail to produce enough energy to sustain cell life. When enough cells cease to function properly organs, motor functions, and the neurological system can become impaired. This chronic and genetic disease affects one in every 4,000 children by the age of 10 in the United States. Mitochondrial disease is often misdiagnosed due to the fact many of the symptoms are synonymous with other, more common, diseases. To learn more about the causes and symptoms of this disease join the Cleveland Clinic in a free web chat with our neurologist and mitochondrial disease specialist, Dr. Sumit Parikh.
Cleveland Clinic Pediatric Neurology ranked in the top four in the country with U.S. News and World Report and ranked No. 1 in Ohio. Each year our world renowned neurologists and neurosurgeons oversee more than 10,000 patient visits. The Pediatric Neurometabolic and Genetic Disorders Program provide diagnosis and treatment for the complex genetic and metabolic disorders that underlie many pediatric neurological and developmental issues, such as mitochondrial disease.
Sumit Parikh, MD, is a neurometabolic and neurogenetics Staff Clinician at Cleveland Clinic. He specializes in the evaluation, diagnosis and treatment of developmental delay, neurodegeneration and metabolic disease. Dr. Parikh is the Co-Director of the Cleveland Clinic Mitochondrial Clinic and the Cyclic Vomiting Syndrome Clinic.
In 2007, Dr. Parikh was selected as one of "America's Best Doctors." He serves as a medical advisor to the United Mitochondrial Disease Foundation and Cyclic Vomiting Syndrome Association. He is a councilor of the Mitochondrial Medicine Society and serves on their Diagnosis Standards and Outreach Committee. He also serves as the Society's website administrator. He is on the scientific planning committee of the Child Neurology Society, and serves on both the Cleveland Clinic Child Advocacy Board and Autism Standards Committee. He is a reviewer for the Journal of Child Neurology.
His clinical interests include the diagnosis and treatment of patients with mitochondrial cytopathies, inborn errors of metabolism, cognitive and developmental regression and developmental delays.
To make an appointment with Dr. Parikh or any of the other specialists in our Pediatric Neurology and Neurosurgery Services at Cleveland Clinic, call toll free at 866.588.2264. You can also visit us online at www.clevelandclinic.org/pediatricneurology
Cleveland_Clinic_Host: Welcome to our Online Health Chat with Dr. Sumit Parikh. We are thrilled to have them here today for this chat. Let’s begin with the questions.
Overview Mitochondrial Disorders
keeptrying: When a mitochondrial disease presents in an adult, does that mean that that person had the problem their whole life, or that it just developed?
Speaker_-_Dr__Sumit_Parikh: It depends. We differentiate between primary (genetic/born-with) mitochondrial disease and secondary mitochondrial dysfunction.
Some individuals have an inherent mitochondrial vulnerability or problem with how their mitochondria work - and the symptoms accumulate over time. Since we have a thousand mitochondria in each cell and a trillion cells - we literally have a gazillion mitochondria. In mitochondrial disease, a person may have a certain percentage of a gazillion not working -> if it is a small percentage -> their symptoms may not begin until later in life or be 'milder.'
Mitochondria are also very vulnerable to damage from other diseases (diabetes), medications (chemotherapy) and toxins (smoking). In these situations, a person may have mitochondrial issues show up after chronic exposure to these offending conditions/agents.
keeptrying: What differences are there, if any, between the way a mitochondrial disorder presents itself in a child versus an adult?
Speaker_-_Dr__Sumit_Parikh: As stated in the prior entry - mitochondrial disorders present differently depending on how severely they are affected. Also - each organ in our body has different pools of mitochondria - and each pool of mitochondria can have varied levels of health as well.
Thus - if a person has many mitochondria affected (of their gazillions) or they are all not working up to speed - symptoms begin early. If the mitochondrial dysfunction is 'milder' or fewer individual mitochondria are affected, symptoms begin later in life.
jheister: Does mitochondrial disease worsen / progress with time, or can it improve?
Speaker_-_Dr__Sumit_Parikh: As one of the previous replies may have alluded to - since there are many types of mitochondrial diseases of varying severity - the answer to your question is that it can do any of these things.
Some patients have chronic symptoms that only worsen during times of medical/physiologic stress. Others can have a slow steady or rapid downhill progression.
keltonCoop: Is there a direct link between life expectancy and the type of mutation present?
Speaker_-_Dr__Sumit_Parikh: As some of you may be picking up - there is no yes/no answer for mitochondrial disease. For life expectancy and mutations, the answer is that it depends on the type of mutation and how many of the 'gazillions' of mitochondria are affected (which we can sometimes quantify when the mutation is known).
platinum: How often do you see mitochondrial disease affecting the immune system?
Speaker_-_Dr__Sumit_Parikh: This topic is still actively being studied. We know that mitochondrial dysfunction leads to more chronic non-life-threatening infections (colds, ear-infections) - and in some patients - having these medical stressors recur frequently leads to a decrease in quality of life.
We do not have a treatment yet though we are more judicious about illness prevention and having an immunologist and infectious disease expert help us with our patients.
Immunoglobulin therapy (a blood product with each dose requiring several thousand donors) is being studied but has not been proven as effective therapy.
hannah: What causes demyelination? Would a high protein diet/ketosis help children with this problem?
Speaker_-_Dr__Sumit_Parikh: Demyelination is a 'generic' word to describe damage to the myelin (coating) around the nerves (whether in the brain or body).
There is no specific diet that helps individuals with demyelination.
johnp: Are Type 1 Fiber Predominance and irregular size muscles fibers the same thing?
hyatt02: My 4 year old daughter has severe diarrhea from the medications she is taking. What can I give her to help with this?
Speaker_-_Dr__Sumit_Parikh: I would defer this question to a gastroenterologist. If the diarrhea is due to supplements (carnitine), lowering the dose and giving it over more intervals (3-4 times a day) and ensuring that you give it with food may help.
If the diarrhea is from dysmotility - a GI doctor can prescribe medication that may help.
Types of Mitochondrial Disorders
gramps: My grandson was recently diagnosed with Complex III Mito Disorder. What is the difference between Type I, II III, IV, V or whatever? Does the higher number mean it is worse? Can a person have more than one?
Speaker_-_Dr__Sumit_Parikh: The various numbers refer to the various portions (departments) in the mitochondria. A higher number is not worse - it just helps physicians know which part of the mitochondria might not be working well and direct genetic testing.
It turns out that these mitochondrial components live meshed together and by having one portion not work properly - another portion may also not work as intended - so yes - a person can have more than one Complex affected.
jackson: I have NARP (Neuropathy, ataxia and retinitis pigmentosa (NARP) syndrome) and associated muscle pain in my legs. I also have joint pain in one knee. Is this related?
Speaker_-_Dr__Sumit_Parikh: Mitochondrial disorders typically do not cause joint injury - though muscle disorders lead to more stress on joints and can exacerbate or bring out a 'minor' joint problem that comes about with 'normal' aging.
junior: I am 48 and was diagnoses with MERRF syndrome (Myoclonus Epilepsy Associated with Ragged-Red Fibers) about 10 years ago, that has been getting progressively worse. I get fatty tumors that have to be removed surgically. Are these tumors related to the MERRF and is there any way to try and prevent their growth?
Speaker_-_Dr__Sumit_Parikh: Fatty tumors (lipomas) can be seen more commonly in certain mitochondrial disorders. There is no way to prevent these.
LHoward: Can you give me any insight into CPEO, such as progression and treatment? Thanks.
Speaker_-_Dr__Sumit_Parikh: CPEO - chronic progressive external ophthalmoplegia - can vary in severity and progression (as can all mitochondrial disorders). The treatment for most mitochondrial disorders is similar -maintaining good health and nutrition, avoiding mitochondrial toxins and considering anti-oxidant supplementation.
dorcie: Is Diffuse Louis Body Disease a form of mitochondrial disease or dysfunction?
Speaker_-_Dr__Sumit_Parikh: Likely leads to secondary mitochondrial dysfunction
Diagnosis of Mitochondrial Disorders
hardymum: How common are misdiagnosis of mitochondrial diseases because they are fairly rare? How would this affect the patient in terms of their treatment?
Speaker_-_Dr__Sumit_Parikh: This is a difficult question to answer. It seems that mitochondrial disorders are not that rare - but we have had difficulty in diagnosing them. Also, the path to diagnosis is complex in that it requires many tests and there is no 'one' test that makes the diagnosis, but rather a person reviewing and interpreting the entire medical picture, or 'clinical story' and lab test results.
What we find too often is that when a patient has symptoms that a diagnosis has not been made for, mitochondrial disorders often get invoked as a diagnosis. We frequently see patients labeled with a mitochondrial disease diagnosis who in fact have something else, whether it be a genetic syndrome, or another medical issue like celiac or Lyme disease.
bobbyG: I have progressive autonomic neuropathy. My doctors have recently been considering doing a muscle biopsy to check for mitochondrial disease. However, they say that even if the test results come back positive for mitochondrial disease, there may be no change in treatment. If so, is it advisable to get the biopsy done?
Speaker_-_Dr__Sumit_Parikh: The muscle biopsy is a stepping-stone to diagnosis. A piece of muscle can get sent for a few or several hundred tests - and it is important to ensure that if mitochondrial testing is being done on muscle, all of the testing is done on it.
There is also an issue of whether a muscle specimen is frozen and sent to a mitochondrial lab for testing vs. obtained in a mitochondrial disease center and then mitochondria are harvested and tested while still living. We suspect that testing living mitochondria is more accurate though this type of biopsy requires a person to travel to Cleveland, Atlanta or San Diego.
Since that is not feasible for many patients, it is more important that ALL the necessary testing to evaluate for mitochondrial dysfunction is obtained the first time the biopsy is done. Far too often, we see that patients receive a muscle biopsy and only 1 or 2 tests are done on it.
It is true though that the muscle biopsy results do not directly affect our ability to provide prognosis or choose treatment if a person has mitochondrial disease. The muscle biopsy is better for helping find mitochondrial dysfunction and potentially directing genetic testing. It is also very useful for helping exclude other conditions that might be treated very differently than if one has mitochondrial disease.
julieB: Is it possible to have different results to muscle biopsies done at different times and by different labs?
Speaker_-_Dr__Sumit_Parikh: YES. This is unfortunately one of the challenges of the field. A piece of muscle, once obtained, can be handled very differently. In addition - each lab often has varied ways of running the testing.
This is one of the reasons why we do not 'rush' into obtaining muscle biopsies - and if we get one - we ensure that select labs are used for the testing.
handmedown: My child was diagnosed with autism. Would you recommend having him tested for a mitochondrial disease? What is the exact correlation between the two?
Speaker_-_Dr__Sumit_Parikh: Most patients who have autism have a genetic non-mitochondrial etiology for their symptoms.
Some patients with autism may have underlying metabolic disease (specifically mitochondrial disease) that may be worsening or bringing out autism and/or other symptoms.
We do not know which patients need to be screened and several groups are actively studying this issue. We suspect that patients with autism and other neurologic issues (seizures or mental retardation), GI dysfunction (chronic diarrhea) or regression after the age of 3 years or with illness may have underlying metabolic issues.
Symptoms of Mitochondrial Disorders
playingaround: What are some of the symptoms that would present themselves that doctors might suspect a mitochondrial disease?
Speaker_-_Dr__Sumit_Parikh: This is a very broad question. I will direct you to the Mitochondrial Medicine Society website (www.mitosoc.org), ‘Toolkit’ section, in-case you would like to read more.
blanketbaby: Is it common for someone with a mitochondrial disorder to show no outward sign that the disorder exists?
playdough: For a Complex I defect, what do you recommend for pain? My son’s pain varies from day to day as to what hurts and severity.
Speaker_-_Dr__Sumit_Parikh: Sadly, our approach to mitochondrial symptoms is the same whether or not someone has mitochondrial disease. Thus, a pain management expert should be able to help - even if they are not familiar with mitochondrial disease. They only need to make sure they do not use medications that have potential mitochondrial toxicity.
nervousmom: Can mitochondrial disease cause behavioral problems in my child?
Speaker_-_Dr__Sumit_Parikh: Possibly. We know that mitochondrial disorders can cause or worsen anxiety, depression, bipolar disease, and autism symptoms.
Pete: When damage to the brain occurs with a mitochondrial disease, is the brain permanently damaged?
Speaker_-_Dr__Sumit_Parikh: Sometimes It depends on how severe the brain injury is. We have had patients have some or complete recovery while others have not.
jheister: Is there a link between mitochondrial disease and crystals found in urine analysis? I read that when muscles break down during an illness / regression that crystals in the urine are an indication. Is that true?
Speaker_-_Dr__Sumit_Parikh: There are MANY causes of crystals in the urine - most being less esoteric than mitochondrial disease. The most common is calcium not being processed in the kidneys properly.
Treatment & Therapies
gold_mom: Is there a complete list somewhere that tells us what medications, IV fluids, anesthetics to avoid because of damage caused to mito?
Speaker_-_Dr__Sumit_Parikh: There is a list of both medications that are used for treatment and ones to avoid available in a Mitochondrial Medicine Society (www.mitosoc.org) paper, published in 2009, called the Modern Treatment of Mitochondrial Disease. More information can be found at the MMS website under the ‘Toolkit’ section.
dorcie: Could statins cause memory loss or muscle atrophy and are there any treatments?
Speaker_-_Dr__Sumit_Parikh: Statins - medications used to treat elevated cholesterol levels - interfere with CoQ10 synthesis. CoQ10 is crucial to mitochondrial function.
We suspect that statins may bring out problems in individuals who had underlying 'mild' or previously silent metabolic muscle disease (mitochondrial or other types).
As far as we know - the only treatment is stopping statins if they are bringing out symptoms and considering CoQ10 supplementation.
jpmorgan: For mitochondrial disease treatment, the levels of vitamins and minerals taken are very high. How does the doctor know when it is too high and instead of helping the body is actually toxic to the body?
Speaker_-_Dr__Sumit_Parikh: We typically follow blood levels of carnitine and leukocyte (white blood cell) levels of CoQ10 when utilizing high doses of these medications.
As a whole, mitochondrial medications have few side effects or toxicities. There is a theoretical concern though that there might be too much of a good thing.
UMDFOhio: I know there are different levels of absorption rates in different medications (CoQ10 for example) is there a specific thing to look for to tell what brand or type is best? My son was on a brand from Integrative Therapeutics but it is no longer available.
Speaker_-_Dr__Sumit_Parikh: There is a lot of debate about this - but Tishcon Corp. has obtained FDA approval for mitochondrial disease because their products have been shown to be bioavailable (available inside the cells) to the FDA's standards.
We understand that this formulation can be costly however, and that the supplement is not covered by insurance. Thus, we have our patients take the form that is most cost-feasible and monitor levels of CoQ in white blood cells to make sure they are getting enough.
plato: I have mitochondrial myopathy. Can massage help with symptoms, or can it hurt?
Speaker_-_Dr__Sumit_Parikh: As a whole - light or therapeutic massage is not harmful. Heavy or deep massage can lead to problems in some patients who turn over or injure their muscle too easily (they typically have elevated blood CPK levels - a marker of muscle turnover).
cranky: I have read somewhere that mito patients should not use aminoglycoside antibiotics. Is this true and if so, which antibiotics are these?
Speaker_-_Dr__Sumit_Parikh: We do try and avoid aminoglycoside antibiotics in patients with known mitochondrial disease. There is a large list of these and your physician(s) should know what these are, though some of them end in -mycin.
dorcie: My physician has increased my dosage of Lipitor® to 20mg daily M-F and 40mg on weekends for increased triglyceride levels, 300 from 246 in 3 months. I am concerned about memory loss. My total cholesterol levels are within normal levels. Should I be concerned about the increased dosage?
Speaker_-_Dr__Sumit_Parikh: We do not suspect statins of causing memory loss in metabolic patients.
Genetics of Mitochondrial Disorders
nervousmom: What are the genetics associated with Mitochondrial Disease? My father had it, I have it and my son has it. If I have more children, will they all have it? How about their children? Does it depend on the disorder or the severity?
Speaker_-_Dr__Sumit_Parikh: This is a very broad question that can have a very long answer.
In brief, mitochondria are made using nuclear DNA (nDNA) blueprints (from mom and dad) and a special DNA blueprint called mitochondrial DNA (mtDNA).
A person with mitochondrial disease may have a mutation (DNA typo) in either nDNA or mtDNA, though 80-90% of the time the problem is in nDNA.
Inheritance of DNA typos can vary in all diseases - including mitochondrial disease. In mitochondrial disease - just having a DNA mutation does not always mean a person will have symptoms.
If you know what DNA mutation is causing mitochondrial disease in your family - an appointment with a genetic counselor would be very helpful.
If a specific DNA diagnosis has not been made, you may want to see a geneticist who specializes in mitochondrial diseases.
jheister: If the son of a mother with mitochondrial disease shows symptoms at birth, it is most likely Primary (genetic) mitochondrial disease? If a daughter of the same mother also shows symptoms (but at age 7) does that mean the father must also have a genetic mutation linked to mitochondrial disease? What type of blood tests would help identify those genes?
Speaker_-_Dr__Sumit_Parikh: It turns out that even in families with the same DNA mutation impairing mitochondrial function (maternally inherited mitochondrial DNA mutations OR nuclear DNA mutations from either mom or dad), each family member may have relatively different symptoms, vastly different severity of symptoms and different ages of onset.
Thus in your case, it is possible it is still the same problem affecting all 3 of you. A geneticist or neurogeneticist with expertise in mitochondrial genetics can help direct you to the correct test - though our ability to make a genetic diagnosis is still limited.
nervousmom: Through my reading, it seems that most of these disorders are passed on through the mother. Is this true?
Speaker_-_Dr__Sumit_Parikh: There is an earlier posting from today that briefly reviews the genetics of mitochondrial disease.
The majority of mitochondrial disorders are inherited or due to new problems in regular (nuclear) DNA (from either mom or dad). Only sometimes is the mitochondrial disorder from maternally inherited mitochondrial DNA disease.
hadto: What difference does genetic testing make when planning for children? Are there some disorders that doctors would recommend not having children? Are there some disorders that can be "fixed" before a child is born if detected in-vitro?
Speaker_-_Dr__Sumit_Parikh: The value of a genetic (DNA) diagnosis is so that the geneticist can discuss with you prognosis (less so for mitochondrial diseases), provide proper preventative care, and guide you as to what the recurrence risk is of this problem happening in any children you have. This may lead to pre-pregnancy or pregnancy related testing.
We do not have an in-vitro fix though for mitochondrial DNA mutations, a mitochondrial DNA 'transplant' is being studied.
Immunizations and Mitochondrial Disorders
nervousmom: I have heard and read that immunizations can be harmful to children with mito disorders. My pediatrician still wants my child to have them. I am undecided. What are your thoughts?
Speaker_-_Dr__Sumit_Parikh: There is no clear evidence that immunizations themselves hurt mitochondrial or metabolic patients.
Medical stress (fever, dehydration, illness, revving up the immune-system) may bring-out or worsen metabolic disorders. Thus, there have been some patients where the fever after an immunization led to symptom onset or worsening. In these individuals - it was not directly the immunization that led to issues.
We recommend that our patients receive immunizations. If they are sensitive to declining during medical stress - spacing out immunizations and tight fever-control may help (but this type of approach is not based in medical science and what physicians call 'anecdotal experience').
Research: Chronic Fatigue and Mitochondrial Disorder
jollymolly: Is there an association between Chronic Fatigue and Mitochondrial Diseases?
Speaker_-_Dr__Sumit_Parikh: The diagnosis of 'chronic fatigue syndrome' is an evolving one. It was recently found that some of these patients may have an underlying retro-viral infection - though more research is still needed to better determine whether this is true.
It is possible that some patients with chronic fatigue have mitochondrial dysfunction - but typically isolated fatigue (and associated issues of chronic pain) are not the only symptoms in mitochondrial disease.
A colleague, Dr. John Shoffner, in Atlanta, is performing research to study the possibility of mitochondrial issues in patients with chronic fatigue syndrome.
Cleveland_Clinic_Host: I'm sorry to say that our time with Dr. Sumit Parikh is now over. Thank you again Dr. Parikh for taking the time to answer our questions about Mitochondrial Diseases.
Speaker_-_Dr__Sumit_Parikh: Thank you so much for joining us today. I appreciate the opportunity in helping answer some of your questions. Have a great day. - Sumit
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The Open Neurology Journal
Bentham Science Publishers
Damage of Collagen and Elastic Fibres by Borrelia Burgdorferi – Known and New Clinical and Histopathological Aspects
Kurt E Müller
Borrelia - bakteeri voi aiheuttaa erilaisia iho-ongelmia mutta myös muutoksia kollageeniin. Siitä puolestaan voi seurata ongelmia jänteissä, selän välilevyissä, nivelsiteissä jne
Lyme Borreliosis, or Lyme’s disease, manifests itself in numerous skin conditions. Therapeutic intervention should be initiated as soon as a clinical diagnosis of erythema migrans is made. The histopathology of some of the skin conditions associated with Lyme Borreliosis is characterised by structural changes to collagen, and sometimes also elastic fibres. These conditions include morphea, lichen sclerosus et atrophicus and acrodermatitis chronica atrophicans. More recently, further skin conditions have been identified by the new microscopic investigation technique of focus floating microscopy: granuloma annulare, necrobiosis lipoidica, necrobiotic xanthogranuloma, erythema annulare centrifugum, interstitial granulomatous dermatitis, cutaneous sarcoidosis and lymphocytic infiltration; these conditions also sometimes cause changes in the connective tissue. In the case of ligaments and tendons, collagen and elastic fibres predominate structurally. They are also the structures that are targeted by Borrelia. The resultant functional disorders have previously only rarely been associated with Borreliosis in clinical practice. Ligamentopathies and tendinopathies, spontaneous ruptures of tendons after slight strain, dislocation of vertebrae and an accumulation of prolapsed intervertebral discs as well as ossification of tendon insertions can be viewed in this light
Nämä oireet löytyvät kehostani mutta ainoastaan kaksi lääkäriä on ne yhdistänyt Borrelia-bakteeriin.
" Hoitamattomassa borrelioosissa 10–50 %:lle potilaista tulee myöhäisoireita muutaman kuukauden, pisimmillään yli vuoden kuluttua puremasta. Oireet ovat moninaisia, iho-, nivel-, hermo-, sydän-, lihas- tai silmäoireita esiintyy vaihtelevasti. Yksi tavallisimmista on kasvohermohalvaus lapsilla ja nuorilla. Myöhäisvaiheen oireet voivat jatkua vuosia (ks. «Krooninen borrelioosi eli krooninen Lymen tauti»1).
Myöhäisvaiheen borrelioosissa esiintyvä iho-oire on hitaasti etenevä surkastuttava ihotulehdus eli acrodermatitis chronica atrophicans (akrodermatiitti). Se oireilee tavallisesti toisessa raajassa alkaen sen kärkiosasta, jalkaterästä tai kädenselästä. Iho muuttuu väriltään sinipunervaksi ja ohenee, ja ihon pinta rypistyy (kuva 5). Raajassa, jossa ihomuutos sijaitsee, voi olla nivelkipua ja turvotusta, poikkeavaa ihon arkuutta tai tunnottomuutta. Pitkälle edenneet akrodermatiittimuutokset eivät korjaannu, vaikka borreliainfektio saadaan hoidettua antibiootilla. "
OLISIKO LYMEN TAUTI LISÄTTÄVÄ ÄÄNIHUULTEN HALVAANTUMISEN SYIHIN?
esittäjä (t): Daniel J. Cameron, MD, MPH
Prevention artikkelissa, lääkärit kuvaavat, miten Lymen tauti voi vaikuttaa henkilön äänihuuliin. ”Lyme voi vaikuttaa hermoihin, jotka ovat vastuussa äänihuulten lihasten hallitsemisesta”, sanoo Amesh A. Adalja, MD, tartuntatautien asiantuntija Johns Hopkinsin terveyskeskuksessa. ”Tämän seurauksena joku voi menettää äänensä teknisesti, jos heillä on Lymen tauti.”
Itse asiassa Journal of Voice -lehdessä julkaistu tapausryhmä tunnisti Lyme-taudin yhtenä äänihuulten halvaantumisen useista syistä, mikä voi vaikuttaa dramaattisesti potilaiden elämään ja vaikuttaa ääni-, nielemis- ja hengitysteiden toimintaan.  Syyn tunnistaminen on tärkeää, kirjoittajat toteavat, jotta he voivat hoitaa onnistuneesti.
Kurkkukipu, äänihuulten halvaus voi johtua neurologisista ja tulehdusolosuhteista sekä erilaisista infektioista. ”Tartuntavaaroja ovat Lymen tauti, Länsi-Niilin virus, varicella, herpes, Epstein-Barr, syfilis ja muut.” 
Vuoden 2016 tapaussarjassa tutkittiin 231 Pennsylvanian potilasta, joilla oli vokaalijohdon halvaus (tai pareseesi). Kirjoittajat totesivat, että syfilis-, myasthenia gravis- ja Lyme-taudin esiintyvyys oli suurempi näillä potilailla verrattuna kansalliseen määrään.
Useilla potilailla, joilla oli äänihuulten halvaus, oli Lymen tauti. ”Viidellä potilaalla (2,2%) havaittiin positiivinen Lyme-tiitteri, jossa oli vahvistava Western-bloti. Kun verrataan 2013 esiintyvyys Lymen taudin Pennsylvania (0,039%), nämä tulokset olivat tilastollisesti merkitseviä (p <0,0001).”
In the Prevention article, doctors describe how Lyme disease can impact a person’s vocal cords. “Lyme can affect the nerves that are responsible for controlling the muscles in the vocal cords,” says Amesh A. Adalja, MD, an infectious disease specialist at Johns Hopkins Center for Health Security. “As a result, someone could technically lose their voice if they had Lyme disease.”
In fact, a case series published in the Journal of Voice identified Lyme disease as one of several causes of vocal cord paralysis, a condition that can dramatically impact patients’ lives, affecting voice, swallowing and airway function.  Identifying the cause is important, the authors state, in order to treat the condition successfully.
sore throat, throat pain, vocal cord paralysisVocal cord paralysis can be caused by infectious, neurologic and inflammatory conditions.
Vocal cord paralysis can be caused by neurologic and inflammatory conditions, as well as by various infections. “Infectious causes include Lyme disease, West Nile virus, varicella, herpes, Epstein-Barr, syphilis, and others.” 
The 2016 case series examined the records of 231 Pennsylvania patients with vocal cord paralysis (or paresis). The authors found that the prevalence of syphilis, myasthenia gravis, and Lyme disease was higher in these patients when compared with the national rate.
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Several of the patients with vocal cord paralysis had Lyme disease. “A positive Lyme titer with confirmatory Western blot was found in five patients (2.2%). When compared with the 2013 incidence of Lyme disease in Pennsylvania (0.039%), these results were statistically significant (P < 0.0001).”