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Old 03-22-2008, 09:52 AM
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More abstracts to share on this complex issue. As I mentioned before, the more provocative studies originate from outside of the U.S., particularly the U.K. and Germany.
__________________________________________________ ___

IS SCIATICA DUE TO BACTERIAL INFECTION?
Journal of Bone and Joint Surgery - British Volume, Vol 87-B, Issue SUPP_III, 291.
Copyright © 2005 by British Editorial Society of Bone and Joint Surgery

Combined Orthopaedic Associations
Sydney, Australia – 24–29 October, 2004 Chairman – Kalev Wilding
A.J. Stirling; M. Jiggins; T.S.J. Elliott; T. Worthington; and P.A. Lambert
The Royal Orthopaedic Hospital Birmingham, UK. The Royal Orthopaedic Hospital Birmingham, UK. Dept of Clinical Microbiology, University Hospital, Birmingham, UK. Dept of Pharmaceutical & Biological Science, Aston University, Birmingham, UK

Introduction and Aims: To confirm whether bacteria were present in disc material harvested at the time of discectomy; and to determine whether the presence of bacteria correlated with elevation of Anti Lipid S antibody levels; and to compare these results with antibody levels and disc specimens from patients undergoing surgery for indications other than radiculitis.

We have previously demonstrated significantly elevated IgG titers (ELISA) to a glycolipid antigen found in the cell wall of most gram-positive bacteria in patients with discogenic sciatica. This raised the possibility that the inflammation associated with disc protrusion might be initiated or accelerated by bacteria.
Method: A prospective study was performed using disc material harvested with stringent aseptic precautions from 207 microdiscectomy and 27 trauma, tumor or scoliosis patients (controls). Serology was obtained for all patients.

Results: In the Microdiscectomy group 76/207 (37%) had positive cultures after seven days incubation, of which 26 (34%) had positive serology. Forty-nine patients had Propionibacteria, 11 Coagulase-negative-Staphylococci (CNS), eight Propionibacteria and CNS, four other organisms and four mixed growth.
One hundred and thirty one (63%) patients had negative cultures of whom 15% had positive serology. There was a significant difference between patients with positive serology and culture, compared with those with negative serology and culture (Fischer exact test P<0.01). In some patients, organisms were visible on microscopy prior to culture. Two of the patients undergoing surgery for other indications had positive cultures (P.acnes) of whom one had positive serology. Of those with negative cultures, six had positive serology. There was a significant difference between positive cultures in those with sciatica and controls (P<.001).

Conclusion: A significant proportion of patients with discogenic radiculitis have positive cultures with low-virulence Gram-positive organisms (predominantly Propionibacteria) and in proportion, a corresponding appropriate antibody response.

These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.

One or more of the authors are receiving or have received material benefits or support from a commercial source.
Modic changes, possible causes and relation to low back pain.
1: Med Hypotheses. 2007 Jul 9; [Epub ahead of print]
Albert HB, Kjaer P, Jensen TS, Sorensen JS, Bendix T, Manniche C.
All The Back Research Center, Part of Clinical Locomotion Science, University of Southern Denmark, Lindevej 5, 5750 Ringe, Denmark.

In patients with low back pain (LBP) it is only possible to diagnose a small proportion, (approximately 20%), on a patho-anatomical basis. Therefore, the identification of relevant LBP subgroups, preferably on a patho-anatomical basis, is strongly needed. Signal changes on MRI in the vertebral body marrow adjacent to the end plates also known as Modic Changes (MC) are common in patients with LBP (18-58%) and is strongly associated with LBP. In asymptomatic persons the prevalence is 12-13%. MC is divided into three different types. Type 1 consists of fibro vascular tissue, type 2 is yellow fat, and type 3 is sclerotic bone. The temporal evolution of MC is uncertain, but the time span is years. Subchondral bone marrow signal changes associated with pain can be observed in different specific infectious, degenerative and immunological diseases such as osseous infections, osteoarthritis, ankylosing spondylitis and spondylarthritis.

In the vertebrae, MC is seen in relation to vertebral fractures, spondylodiscitis, disc herniation, severe disc degeneration, injections with chymopapain, and acute Schmorl's impressions. The aim of this paper is to propose two possible pathogenetic mechanisms causing Modic changes. These are: A mechanical cause: Degeneration of the disc causes loss of soft nuclear material, reduced disc height and hydrostatic pressure, which increases the shear forces on the endplates and micro fractures may occur. The observed MC could represent oedema secondary to the fracture and subsequent inflammation, or a result of an inflammatory process from a toxic stimulus from the nucleus pulposus that seeps through the fractures. A bacterial cause: Following a tear in the outer fibers of the annulus e.g. disc herniation, new capilarisation and inflammation develop around the extruded nuclear material. Through this tissue it is possible for anaerobic bacteria to enter the anaerobic disc and in this environment cause a slowly developing low virulent infection. The MC could be the visible signs of the inflammation and oedema surrounding this infection, because the anaerobic bacteria cannot thrive in the highly aerobic environment of the MC type 1.

Perspectives: One or both of the described mechanisms can - if proven - be of significant importance for this specific subgroup of patients with LBP. Hence, it would be possible to give a more precise and relevant diagnosis to 20-50% of patients with LBP and enable in the development of efficient treatments which might be antibiotics, special rehabilitation programmes, rest, stabilizing exercise, or surgical fixation, depending on the underlying cause for the MC.
PMID: 17624684 [PubMed - as supplied by publisher]

1: Clin Orthop Relat Res. 1992 Jul;(280):175-8.
Case report of an unusual cause of low back pain. Intervertebral diskitis caused by Eikenella corrodens.
Noordeen MH, Godfrey LW. Department of Orthopaedic Surgery, Stoke Mandeville Hospital, Aylesbury, Buckinghamshire, England.

A 42-year-old man suffered from low back pain caused by intervertebral diskitis. The condition was diagnosed on plain roentgenogram and computed tomography scans. The infected area was biopsied and grew Eikenella corrodens, a gram-negative anaerobic rod, which grows slowly only after culture on blood agar in 5-10% carbon dioxide. This is the first reported case of E. corrodens intervertebral diskitis causing acute low back pain. Recognition of this organism in this condition emphasizes the importance of aerobic and anaerobic cultures of infected disks. The organism has unusual antibiotic sensitivities. The infection, once appropriately treated, responded rapidly.
Bacterial Pathogenesis and Genomics Research Grouphttp://www.ciir.qub.ac.uk/bpg/bpgfront.htm

Research within this group centres on infection caused by obligately anaerobic bacteria. There are two main areas of interest. Firstly bone and joint infection, focusing on prosthetic joint failure, fracture healing and the possible role of bacterial infection in sciatica and back pain. Previous studies from this group indicate that the bacterium Propionibacterium acnes is frequently associated with failed artificial hips. Therefore studies of the virulence determinants of this bacterium may give key insights into the relationship between infection and the osteolysis that leads to artificial hip failure. The second main area of interest relates to opportunistic infection arising from the normal intestinal microbiota, such as peritonitis, the risk of which requires prophylactic antibiotic treatment prior to bowel surgery. Bacteroides fragilis is a major cause of this type of infection. The Wellcome Trust have recognised the importance of this pathogen and are funding the complete genome sequencing programme, which is a joint project between the Sanger Centre, Cambridge UK and Dr Patrick’s laboratory. This opens up exciting possibilities with respect to the study of B. fragilis pathogenesis.

'This group is a member of the Research and Development Office of the HPSS Northern Ireland, Infectious Diseases Recognised Research Group from whom S Patrick has a 5 year Programme Grant. Additional current funding sources include the British Orthopaedic Wishbone Trust, the Royal College of Surgeons of England and the Department of Employment and Learning NI. Current collaborative links include the Schools of Biology & Biochemistry, Agriculture & Food Science and Pharmacy at QUB; Orthopaedic Surgery, Musgrave Park Hospital & the Royal Victoria Hospital NI; the Sanger Wellcome Institute, Cambridge; the Institute of Cell and Molecular Biology, University of Edinburgh and the University of Capetown, SA.'

Doctors stumble on infection clue to sciatica cure

By Lorraine Fraser, Medical Correspondent
Last Updated: 11:54pm BST 14/07/2001

DOCTORS believe that half of all cases of the excruciating back pain known as sciatica could be caused by an infection which is easily cured by antibiotics.Specialists in Birmingham have found slow-growing bacteria of the kind that normally lives on the surface of the skin in spinal tissue from nearly 50 per cent of patients with sciatica.

The finding suggests that a course of antibiotics could be all that is needed to solve the problem for millions of sufferers, revolutionising the way that doctors treat back pain. A clinical trial involving hundreds of patients is being set up to test the hypothesis and the results should be known in 18 months' time. The NHS spends £500 million a year on investigations and therapy for patients with back pain, which is one of the most difficult complaints to treat.

The cost to industry in terms of lost working time is an estimated £4 billion annually and the potential savings, should the doctors be proved right, would be enormous.

Tom Elliott, the professor of clinical microbiology at the University Hospital in Edgbaston, told The Telegraph that the finding of infection in patients with sciatica was "very exciting".
He said: "In terms of future therapy it may mean we could treat this with antibiotics. It could have a tremendous impact in terms of the management of patients with back pain and that has large implications for the NHS as a whole."

Sixteen million people suffer at least one bout of back pain in the UK in any one year and sciatica - pain in the sciatic nerve which extends down the leg from the base of the spinal cord - is one of the most common symptoms.

It has traditionally been explained as pressure on the sciatic nerve from a bulging or "slipped" vertebral disc.
However, until now there has been no explanation for the inflammation which is frequently present.
Professor Elliot and four colleagues from Aston University and the Royal Orthopaedic Hospital in Birmingham stumbled across the answer when trying out a blood test for deep-seated infections in patients, intended to identify infections of the heart or bone.

They applied the test to sciatica sufferers as a "control" group expecting negative results in these individuals - only to find that in a third of them it was positive.

They have examined disc tissue from 180 patients with sciatica so severe that they needed surgery and found bacterial infection in 46 per cent of them.

The most frequently occurring microbe was Proprionibacterium acnes, a normal skin bacterium linked to acne.
Professor Elliot said: "We think the organisms are getting into the blood and settling in this part of the body, perhaps in already damaged discs, setting up a low-grade infection."

The theory would explain why some people have slipped discs but do not have sciatic pain. The bacteria concerned are all sensitive to common antibiotics. Tests are under way to see if it is possible to get sufficient drug into the infected discs to kill the bacteria.

Professor Elliot said: "We suspect that short courses of antibiotics won't work and sciatica patients may need six weeks of antibiotics, as is the case for example in bone infection."
In future it might also be possible to use the blood test to spot those who might benefit from antibiotic treatment, he added.

A spokesman for the charity BackCare, which helped to fund the research, said: "This is extremely interesting work and we will be very excited to see the results of the clinical trial, but we must wait and see."

http://www.telegraph.co.uk/news/main.jhtml?xml=/news/20...1/07/15/ixhomef.html
Language: German English title: Neuro-borreliosis or intervertebral disk prolapse?
Authors: Dieterle, et al

Abstract: Between September 1986 and November 1988, 17 patients were hospitalized and treated for neuro-borreliosis. Ten of them had been admitted with suspected lumbar or cervical root or compression syndrome. Only four patients recalled a tick bite, only three an erythema migrans. Uni- orbilateral facial paresis was a prominent feature in six patients. Three of 14 patients had no IgG antibodies against Borrelosis, either in serum or cerebrospinal fluid at the initial examination, two had positive serum in titers only. Despite antibiotic treatment (usually 10 mega U penicillin threetimes daily) six patients had recurrence by April, 1989. treated with penicillin again or with twice daily 100 mg doxycycline or2 g ceftriaxon. In four of them a residual painful polyneuropathy remains.

Author: Meier, et al
title : Meningoradiculitis mimicking vertebral disc herniation . A "neurosurgical " complication of Lyme-borreliosis.
source: Acta Neurochir: (Wien) 1989;98(1-2):42-6

Abstract: We report on 3 patients with meningoradiculoneuritis (MRN) due to Lyme-borreliosis (LB)., which presented clinically as vertebral disc herniation. In 2 cases the undelying infection was discovered only after UNSUCESSFUL NEUROSURGICAL TREATMENT. In the differential diagnosis between MRN and disc herniation the following criteria are suggestive of MRN and should raise suspicion of a non-discogenic aetiology: History of tick bite or erythema chronicum migrans, fever or general malaise, mono-or ligoradiculopathy with absent or insignificant lumbar pain and complaints of a burning character of the radiating pain. In suspicious cases we recommend blood investigations including antibody determination against borrelia burgdorferi and CSF investigations including cell count and cytology, protein and glucose determination, nephelometry and isoelectric focusing to exclude MRN and other conditions that may mimic disc herniation.

Neurologic Manifestations of Lyme Disease, the New Great Imitator
author: Andrew Pachner
source: Review of Infectious Diseases Vol. 11, supplement 6 Sept-Oct 1989

"....A Washington D.C. business executive had developed pain in both his shoulders and arms. The pain described as aching or gnawing and sometimes electrical, was worse on the left side. A diagnosis of cervical disk disease was made, and a number of remedies appropriate for such a diagnosis were attempted. None was sucessful. Subsequent computed tomography and magnetic resonance imaging of the cervical spine revealed a small right C5 disk. The patient's discomfort was attributed to this disk despite the fact that he had bilateral symptoms that were more severe on the contralateral.......serologic studies for Lyme disease
were performed. The result was positive....A positive Lyme serology was confirmed in my lab...therapy with intravenous penicillin..was begun. The patient has done well, with resolution of his pain and no progression of his disease...."

Incidence of nervous system Borrelia burgdorferi infection in patients with lumboradicular syndrome.

Authors:Schmutzhard E, Mohsenipour I, Stanek G
Source:Eur Neurol 1993;33(2):149-51
Organization: Department of Neurology, University Hospital Innsbruck, Austria.

We investigated 103 consecutive patients primarily admitted to our Department of Neurosurgery (36 women, age: median 44, range 21-79; 67 men, age: 47, range 19-77) suffering from low back pain radiating into one or both legs. Neurological examination combined with computer tomography and lumbar myelography revealed lumbar-disc herniation in 74, vertebrostenosis in 10 and relapsed disc herniation in 9 patients. In 9 patients the diagnosis of pseudoradicular syndrome was established without definite neuroradiological morphological evidence. Two patients were diagnosed as having polyneuropathy, and 1 patient suffered from a nervus ischiadicus lesion due to a gluteal abscess. CSF of all patients was examined according to a fixed routine schedule (cells, protein, sugar, immunoglobulins, IgG index). Antibodies to Borrelia burgdorferi were found in the serum and CSF of 5.8%, and in the serum alone of 2% of patients. Intrathecally produced specific antibodies were detected in 3 patients (2.9%) with neuroradiological evidence of disc or spinal-canal disease, indicating the coexistence of previous CNS infection by B. burgdorferi with lumbar-disc herniation. None of the patients showed CSF pleocytosis; thus, in no case was acute radiculitis due to B. burgdorferi infection diagnosed.

Language: Eng Unique ID: 93223723

Meningoradiculoneuritis mimicking vertebral disc herniation. A "neurosurgical"
complication of Lyme-borreliosis.

Authors:Meier C, Reulen HJ, Huber P, Mumenthaler M
Source:Acta Neurochir (Wien) 1989;98(1-2):42-6
Organization:University Department of Neurology, Inselspital, Bern,
Switzerland.

We report on 3 patients with meningoradiculoneuritis (MRN) due to Lyme-borreliosis (LB), which presented clinically as vertebral disc herniation. In 2 cases the underlying infection was discovered only after unsuccessful neurosurgical treatment. In the differential diagnosis between MRN and disc herniation the following criteria are suggestive of MRN and should raise suspicion of a non-discogenic aetiology: History of tick bite or erythema chronicum migrans, fever or general malaise, mono- or oligoradiculopathy with absent or insignificant lumbar pain and complaints of a burning character of the radiating pain. In suspicious cases we recommend blood investigations including antibody determination against borrelia burgdorferi and CSF investigations including cell count and cytology, protein and glucose determination, nephelometry and isoelectric focusing to exclude MRN and other conditions that may mimic disc herniation.

Language: Eng Unique ID: 89300369
_________________

Meningopapillitis disclosing Lyme disease
Authors:Gerard P, Canaple S, Rosa A
Source:Rev Neurol (Paris) 1996 Jun-Jul;152(6-7):476-8
Organization:Service de Neurologie, CHU Amiens.

Abstract:
A 65 old year woman was admitted to the hospital for a low back pain, a fever and an elevated sedimentation rate. Four months later she noted a progressive visual loss first affected the right eye (visual acuity: 6/10) and then the left (visual acuity : 6/10). Fundus examination showed a bilateral papilledema.

CT Scan and MRI were normal. A lumbar puncture disclosed a lymphocytic pleocytosis (68 leukocytes/mm3), an increase in protein level (1,9 g/l) and oligoclonal bands. A serologic test for B. Burgdorferi was positive both in blood (1/64 degrees) and n cerebrospinal fluid (> or = 1/128). The patient was treated with intravenous ceftriaxone 2 g daily for 2 weeks. Fifteen days later the low back pain had disappeared and the CSF cellular count had decreased to
20 leukocytes/mm3. Seven months later, CSF was normal (2 leukocytes/mm3, protein level: 0.65 g/l.); Titer against B. Burgdorferi had improved to 1/160 in serum and 1/16 in CSF; visual acuity had improved to 8/10 on left, and was the same on right.

Language: French Unique ID: 97099678

Clinical And Electrophysiologic Findings In Chronic Neuropathy Of Lyme Disease.
Authors:Logigian EL, Steere AC
Source:Neurology 1992 Feb;42(2):303-11
Organization: Department of Neurology New England Medical Center Boston MA.

We evaluated 25 patients with Lyme disease and chronic peripheral neuropathy. All had immunologic evidence of exposure to Borrelia burgdorferi and no other identifiable cause of neuropathy. Neuropathic symptoms began a median of 8 months (range, 0 to 165) after erythema migrans and had been present for a median of 12 months (range, 2 to 168) prior to evaluation. Twelve patients (48%) had generally symmetric distal, nonpainful paresthesia, and another 12 (48%) had generally asymmetric radicular pain. One patient (4%) had
asymptomatic neuropathy. The most common physical finding was multimodal sensory loss, which was observed in 13 patients (52%); weakness and hyporeflexia were less common. Motor or sensory nerve conduction was slightly slow in 16 patients (64%). The paresthesia group more often had abnormalities on physical examination and on nerve conduction testing than did the radicular group. In 75% to 80% of patients from both groups, however, needle examination showed denervation in paraspinal and limb muscles. Among 20 patients who
underwent lumbar puncture, only one had a slight spinal fluid pleocytosis. Six months after treatment with intravenous ceftriaxone, 19 patients (76%) were clinically improved. We conclude that Lyme disease can be associated with a reversible, mild chronic axonal sensorimotor polyradiculoneuropathy or polyradiculopathy.

Language: German Unique ID: 92140650

Persistent Leg Pain (clinical conference)
Authors:Satz N, Dvorak J, Reich C, Knoblauch M
Source:Schweiz Rundsch Med Prax 1990 Jul 3;79(27-28):886-8
Organization:Medizinische Abteilung Kreisspital M:annedorf, Z:urich.

A 72 year old patient suddenly experienced severe lumbar pain irradiating into the right leg. Later on, weakness of the muscles thigh appeared. A thorough radiological investigation which showed degenerative alterations of the vertebral column did not supply an explanation. After a pathological titer against Borrelia burgdorferi was found in serum and radiculitis was detected on EMG, the diagnosis of Lyme-Borreliosis of the nervous system could be confirmed by analysis of the cerebrospinal fluid. Under intravenous antibiotic treatment with Ceftriaxone (2 to 4 g daily for three weeks) the symptoms regressed completely, and the pathological findings in the CSF regressed. The significance of some findings in CSF in relation to Borreliosis of the CNS.
Localization of Borrelia Burgdorferi in the Nervous System And Other Organs In A Nonhuman Primate Model Of Lyme Disease.
Cadavid D, O'Neill T, Schaefer H, Pachner AR.
Department of Neuroscience, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA.

Lyme borreliosis is caused by infection with the spirochete Borrelia burgdorferi. Nonhuman primates inoculated with the N40 strain of B. burgdorferi develop infection of multiple tissues, including the central (CNS) and peripheral nervous system. In immunocompetent nonhuman primates, spirochetes are present in low numbers in tissues. For this reason, it has been difficult to study their localization and changes in expression of surface proteins. To further investigate this, we inoculated four immunosuppressed adult Macaca mulatta with 1 million spirochetes of the N40 strain of B. burgdorferi, and compared them with three infected immunocompetent animals and two uninfected controls. The brain, spinal cord, peripheral nerves, skeletal muscle, heart, and bladder were obtained at necropsy 4 months later. The spirochetal tissue load was first studied by polymerase chain reaction (PCR)-ELISA of the outer surface protein A (ospA) gene. Immunohistochemistry was used to study the localization and numbers of spirochetes in tissues and the expression of spirochetal proteins and to characterize the inflammatory response. Hematoxylin and eosin and trichrome stains were used to study inflammation and tissue injury. The results showed that the number of spirochetes was significantly higher in immunosuppressed animals. B. burgdorferi in the CNS localized to the leptomeninges, nerve roots, and dorsal root ganglia, but not to the parenchyma. Outside of the CNS, B. burgdorferi localized to endoneurium and to connective tissues of peripheral nerves, skeletal muscle, heart, aorta, and bladder. Although ospA, ospB, ospC, and flagellin were present at the time of inoculation, only flagellin was expressed by spirochetes in tissues 4 months later. Significant inflammation occurred only in the heart, and only immunosuppressed animals had cardiac fiber degeneration and necrosis. Plasma cells were abundant in inflammatory foci of steroid-treated animals. We concluded that B. burgdorferi has a tropism for the meninges in the CNS and for connective tissues elsewhere in the body.

Curr Treat Options Neurol. 2006 May;8(3):179-84
Ehrlichia Infection of The Central Nervous System. Hongo I, Bloch KC.
Division of Infectious Diseases, Vanderbilt University School of Medicine, A-2200 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232, USA. igen.hongo@vanderbilt.edu
Ehrlichiosis in the United States is caused by three closely related bacterial species (Ehrlichia chaffeensis, Ehrlichia ewingii, and Anaplasma phagocytophilum), all transmitted through tick bite. Although there is variation with respect to geography and tick vector, the clinical manifestations are similar, and treatment of these infections is identical. Ehrlichiosis can present with a spectrum of neurologic manifestations, ranging in severity from headache to meningoencephalitis. Treatment is straightforward if the diagnosis is suspected, but antibiotic therapy should not be delayed pending laboratory confirmation. Doxycycline, the treatment of choice for adults and children with suspected ehrlichiosis, has high bioavailability and can be administered orally in most cases. Therapy is typically continued at least 3 days after the last documented fever. Although there have been no studies specifically evaluating duration or dosing of doxycycline for Ehrlichia meningoencephalitis, anecdotal reports suggest 100 mg doxycycline administered twice daily is effective, despite limited penetration into the cerebrospinal fluid. Because doxycycline interacts with CYP3A4 enzymes, there is potential for drug interactions with a number of medications. In endemic areas, documentation of coinfection with Borrelia burgdorferi, the etiologic agent of Lyme disease, may require prolonging the duration of doxycycline therapy.
PMID: 16569376 [PubMed]

1: Przegl Epidemiol. 2006;60 Suppl 1:125-30.
Diagnosis and Treatment of Lyme Arthritis [Article in Polish]
Przytuła L, Gińdzieńska-Sieśkiewicz E, Sierakowski S.
Klinika Reumatologii i Chorób Wewnetrznych AM w Białymstoku.

Lyme disease is a multisystem disease that affects primarily skin, nervous system, heart and joins. Lyme disease is caused by Borrelia burgdorferi and spread by Ixodes ticks. Arthritis is a well-known manifestation of Lyme disease (LD). Joint symptoms associated with B. burgdorferi infection range from arthralgias, to brief attacks of arthritis, to chronic erosive synovitis. Arthritis may present as oligo- or monoarthritis and typically causes intermittent attacks of oligoarticular arthritis in a few large joints, especially the knee. A small percentage of patients may develop chronic arthritis. The diagnosis is usually based on the clinical picture, exposure in an endemic area, and detection of IgG antibody against B. burgdorferi by ELISA and Western blotting. Spirochetal DNA may be detected in joint fluid by PCR. Antibiotic treatment during early stages normally prevents development of late manifestations. Joint involvement is treated successfully with a 1-month course of doxycycline or ceftriaxone. However, about 10% of Lyme arthritis patients do not respond sufficiently to antibiotic treatment. If patients have persistent arthritis despite a second course of antibiotics with negative results of PCR testing, treatment with anti-inflammatory agents or arthroscopic synovectomy is possible. In this article, we discuss clinical features, diagnosis and treatment.
PMID: 16909789 [PubMed - indexed for MEDLINE]

Scand J Infect Dis. 2007 Jul 6;:1-3 [Epub ahead of print]
Group G Streptococcus Spinal Epidural Abscess: Case Report and Review of The Literature. Saeed MU, Gottmukkula R, Kennedy DJ.
From the Department of Infectious Diseases, Saint Louis University Hospital, St. Louis, Missouri, USA.
Group G streptococci have been identified as a recently emerging pathogen. Spinal epidural abscess is an infrequent but well described infection of the central nervous system that may present with non-specific clinical symptoms and physical examination findings. Group G streptococci are a rare cause of spinal epidural abscess that should be considered in the clinical picture so that appropriate therapy can be initiated in a timely fashion.
PMID: 17852916 [PubMed - as supplied by publisher]

Neurologia. 2007 Jun 28; [Epub ahead of print]
Past Hepatitis B Virus Infection And Demyelinating Multiphasic Disease: Casual or Causal Relationship? [Article in Spanish]
Santos D, Arias-Rivas S, Dapena D, Arias M.
Servicio de Neurología. Hospital Clínico Universitario. Santiago de Compostela.
Introduction. The relationship between hepatitis B virus and hepatitis B vaccine with central nervous system demyelinating diseases is controversial. Case reports. We describe two male patients, who in their 70's developed recurrent pictures of acute demyelinating diseases. The first one had recurrent acute disseminated encephalomyelitis (diplopia, paraparesis and urinary retention) and the second one recurrent transverse myelitis (paraparesis and urinary retention).
Results. The cerebrospinal fluid test showed mononuclear pleocytosis with negative oligoclonal bands in both patients. Visual evocated potentials were normal. Magnetic resonance imaging (T2-WI and FLAIR) showed hyperintense lesions located in the brain and spinal cord in the first case and only in the spinal cord in the second. With negative antigenemia, antibodies against hepatitis B core and hepatitis B surface antigens were positive in both patients. No patient had been vaccinated for nor had suffered symptomatic hepatic disease. In the second patient, there was an almost total remission of the symptoms with periodic treatment with immunoglobulin.
Conclusions. We recommend hepatitis B virus infection investigation in all patients with central nervous system demyelinating disease. Neurología 2007;22(0):0-0.
PMID: 17602335 [PubMed - as supplied by publisher]

PMID: 17554701 [PubMed - indexed for MEDLINE]
Spinal Brucellosis: Turkish Experience Based On 452 Cases Published During The Last Century.
Turgut M, Turgut AT, Koşar U.
Department of Neurosurgery, Adnan Menderes University School of Medicine, Aydin, Turkey. drmturgut@yahoo.com
BACKGROUND: Spinal brucellosis continues to be the leading cause of morbidity from infectious disease in the infested regions of the world, particularly in the rural areas including Turkey. The purpose of this review was to present the Turkish experience by analyzing the literature on the management of spinal brucellosis during the last century.
MATERIALS AND METHOD: To establish new guidelines for the diagnosis and treatment of this disabling health problem, publications reported from Turkey in national (n = 27) and international (n = 37) journals during the last century and databases containing medical literature were analysed.
RESULTS: It was observed that the number of articles produced by Turkish authors regarding spinal brucellosis has tremendously increased throughout the study period. Although the total number of reported cases with spinal brucellosis from a total of 34 secondary or tertiary referral centers in Turkey was 452, only cases having detailed information were evaluated for further analysis according to inclusion/exclusion criteria. Despite the inherent limitations, this type of study clearly indicates that the incidence of brucellosis has not decreased in Turkey over recent years. The clinical and radiological findings of brucellosis involving the spine were mostly atypical and it was difficult to diagnose this infectious disease owing to its nonspecific and variable clinical picture. Therefore, it may easily lead to a misdiagnosis of lumbar disc herniation or other spinal infections and a high index of suspicion is required to diagnose this condition in endemic parts of the world. In addition to serological tests, CT and/or MRI techniques were found to be sensitive for diagnosis and follow-up because they provide early diagnosis of lesions involving the spine and more accurate localization of intraspinal and paraspinal infestation by means of multiplanar images. Histologically, noncaseating granulomatous tissue and chronic inflammation were characteristic features of cases of brucellosis with spinal involvement.
CONCLUSIONS: Based on this critical review of literature from Turkey, it is concluded that early diagnosis and correct management are important to prevent the harmful effects of brucellosis and its complications, and that the treatment of choice is antibiotic therapy alone in most cases of brucellosis involving the spine.

PMID: 16944052 [PubMed - indexed for MEDLINE]
Acta Med Port. 1992 Sep;5(8):419-23.
Spinal Brucellosis. 4 Years Of Experience [Article in Portuguese]
Lopes C, Oliveira J, Malcata L, Pombo V, Da Cunha S, Côrte-Real R, Meliço-Silvestre A.
Clínica de Doenças Infecciosas dos Hospitais, Universidade de Coimbra.
The Authors retrospectively studied 17 patients who have been admitted to the Infectious Diseases Clinic of Coimbra University Hospital during a four year period and whose final diagnosis was brucellar spondylitis. Clinical, epidemiological, laboratory and imaging features are analyzed, as well as those related to the therapeutic schedules and outcome. Females were more often affected (70.58%) and the mean age was 53.35 +/- 13.82 years. Lumbar spine was most frequently involved and an unusual elevated incidence of paravertebral soft tissue swelling was noticed (23.52%). Two patients were also suffering from neurobrucellosis (11.76%). The preferred therapeutic schedule was rifampin and doxycycline and surgery was performed in one patient. Finally, several comments are made regarding basically the incidence, laboratory and imaging diagnosis, therapeutic aspects and evolution of the disease. The imaging similarities and differences between tuberculous, pyogenic and brucellar spondylitis are briefly approached.

PMID: 1442190 [PubMed - indexed for MEDLINE]
Radiologic Findings of the Lumbar Spine in Patients with Rheumatoid Arthritis, and a Review of Pathologic Mechanisms.
Journal of Spinal Disorders & Techniques. 16(1):38-43, February 2003.
Kawaguchi, Yoshiharu; Matsuno, Hiroaki; Kanamori, Masahiko; Ishihara, Hirokazu; Ohmori, Kazuo; Kimura, Tomoatsu

Summary: We have analyzed the radiologic findings on the lumbar spine and the clinical symptoms in patients with rheumatoid arthritis (RA). A total of 106 patients who fulfilled the revised criteria of the American Rheumatism Association were subjected. All of the patients were asked to fill out a questionnaire about the existence of low back pain, leg pain, and leg numbness. Radiologic features of the lumbar spine, including scoliosis, spondylolisthesis, disc space narrowing, endplate erosion, osteophyte, and osteoporosis, were checked. Radiographs of the cervical spine were also taken. The clinical background of RA, such as mutilating disease or not, was assessed. Forty-two patients (40%) had the symptoms of low back pain. Abnormal radiologic findings in lumbar spine were detected in 57%. The prevalence of clinical symptoms tended to be higher in the patients with endplate erosion. Forty-two percent of the patients had both lumbar and cervical lesions. The prevalence of lumbar lesion was not high in the mutilating type of RA, except for facet erosion and severe osteoporosis. The patients with pulse steroid therapy revealed a higher prevalence of vertebral fracture. From these results, we concluded that lumbar lesions were frequently observed in patients with RA. The possibility of lumbar lesions as well as the lesions in the cervical spine and peripheral joints should be examined in patients with RA.
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Old 04-22-2008, 07:30 AM
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Continuing to update this topic here...a UK spine patient sent me a link to this 12-year-old paper.
_____________________________________

Isolated neuritis of the sciatic nerve in a case of Lyme disease
Journal The Italian Journal of Neurological Sciences

Publisher Springer Milan
ISSN 0392-0461 (Print) 1126-5442 (Online)
Issue Volume 19, Number 2 / April, 1998

Case Report

Isolated neuritis of the sciatic nerve in a case of Lyme disease

S. Avanzi1 G. Messa1, A. Marbini1, G. Pavesi1 and F. Granella1
(1) Institute of Neurology, University of Parma, Strada del Quartiere 4, 1-43100 Parma, Italy
Received: 2 December 1996 Accepted: 14 February 1998

Abstract Lyme disease is an infectious disease caused by the spirochete Borrelia burgdorferi. The course of the disease is divided into three stages, the second of which may include various types of peripheral nervous system disturbances. We report the case of a patient with persistent deficits caused by the prevalent involvement of the sciatic nerve, confirmed by electrophysiological and neuropathological findings. The most significant bioptic results were axonal degeneration and perivascular inflammation. Damage to a single peripheral nerve as the dominant clinical expression during the course of Lyme disease is an unusual finding that has been rarely described in the literature.

Key words Lyme disease - Peripheral neuropathy - Sciatic nerve - Nerve biopsy - Vasculitis
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Old 05-16-2008, 04:44 PM
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Just bumping this to the top -- especially for the new UK patient I just spoke with a few moments ago...
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Old 05-19-2008, 02:10 PM
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This is a really interesting article on reactive arthritis. For those of you that may have unusual pain syndromes (before AND/OR after surgery), please read these carefully!

http://www.drmirkin.com/joints/J103.htm

No, not everyone actually has ankylosing spondylitis -- but the overall context of all these articles in this topic illuminate the gaping hole in spinal diagnostics.

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Old 06-09-2008, 07:47 PM
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This is most interesting- I need to read more about this - especially since over the years I have had "odd" neurological and pain events - when I did not have a herniated disk and little to no DDD. Now - I do have a herniated disk that is abutting (well- probably compressing to some degree the cord - will know more next week).

I understand stress plays a big role with these "pathogens" to increase the inflammation -my body has "fallen" apart after several major stressful events in my life. I dont want to bore you with my story - but - if gives you an idea why the drs are a bit puzzled:

pain/numbness in my left hand back in 1989 in college (not that this should be stressful) - to the point where I could not use it for a full semester(I am left handed - a problem). Then out of the blue - it cleared up - and it was really challenged in post grad school (which was stressful) - but no problems -thankfully.

In 2002 - just few years after my Mom died and some other very stressful issues at the time- I had 5 mos of a horrible body break down episode - both hands - very numb, severe neck and shoulder pain, facial numbness, and lower back pain, sciatica - with numbness into my left leg - and my left toe would go numb (which I have having again now). All MRIs and emgs wre normal (except for a problem with the left tricep which could explain the left hand problem in 1989. Drs - thought it was carpel tunnel and stress. Finally- the body rebounded - (I think I was on alot of antibiotics at the end of that year due to recurring sinus infection). Felt great - and went back on to life with occasional numbness in the hands - which a good massage would take care of for the shoulders. Many sinus infections and alot of antibiotcis.

Ffast forward to 2005. Just a week after losing my Dad - (again another major stress event) - the body fell apart. Numbness in the face all over the body (including that left big toe....again), chest pain, and pain - in many places, that left toe went numb too, etc. I regret that they did not do an MRI on my neck (which I wanted) but they were worried it was either my heart (I had chest pains) or a brain tumor - MRI on brain was clear - so were heart exams. Body rebounded felt great. Would have neck pain and stiffness - treated by the chiro- and

fast forward to Aug 2007. Alot of stress going on - at the office, and in personal life. Body breakdown again. This time severe numbness - everywhere - mostly on the left side - gait issues, leg pain (left toe would go numb) also the soles of my feet, pain like I have never suffered before, could not use neck very well, facial numbness, jaw pain, etc. MRI on the neck - showed DDD at C5-6 - protruding and abutting the cord right central - mild stenosis. (Some drs did not feel there was any abuttment). Lumbar - small tear at L4-5, throastic - normal. Brain MRI normal. EMG/nerve conduction tests- normal. I went full guns for testing this time! Finally - after 4 mos of intense pain and numbness (mostly on the left side), horrible traction which made the pain worse, PT, accupuncture, and alot of celebrex - the body rebounded again. One dr thought I had fibro....I did not have the range of motion on my neck I used to have - but my body was "calm" and not on high alert/traffic mode. I also was back on antibiotics late last fall....Not sure if that is the link to rebounding...

I know that I now have a spine issue - that if not treated will get worse and lead to more spine damage -which I do not want to get to. But - I went to some of our "top drs" here in Florida last fall searching for answers - and they were mystified at my symptoms. No surgery was recommended last fall. I dont believe I have MS - the MRIs were clean (while I knowthat is not the complete answer for diagnosis - but a good indication from what I have been told). But - it does beg the question - if I had no stenosis in 2002 and 2005 - then why did I have those strange numbness/pain episodes? I was just told last week by a local neurologist that I have an unexplained neurological syndrome. That is not good enough answer! So - perhaps I have 2 issues going on - one with the spine -and this other type of immune issue which may have led to the spine deterioration....

And again - a few stressful episodes of late - and a minor jerk of the neck (I forgot all about my structural instability - I was feeling that great) - and bam - the wave of pain, numbness - and yes - the big toe on the left foot are all back. Back on celebrex, PT, and new cervical MRI....I suspect that there has been a slight deterioraton in the disk....

Off to get a bunch of blood tests I think is the next approach while poundering what to do to correct my current situation. I pray I can hold off on surgery - as I know they are developing some wonderful new technologies but will have to see..

Sorry to bore you with all of this! But reading about those immune issues - I had to share.
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Aug 2007 - diagnosed with DDD at C5-6 - herniated disk with mild stenosis at right/central of cord - but pain/occasional numbness mostly on the left side - and down into the leg/foot - which has puzzled doctors - even had a lumbar puncture - but thankfully all clear!
May 2008- after many months of no symptoms and issues- flare up- and new MRI shows moderate stenosis.
L4-5 small annular tear with some DD
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Old 06-13-2008, 06:53 AM
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Twix, this is not boring at all. On the contrary -- it's validation. This year, about half the patients I've spoken to on the phone recall a time in their lives when they had some other serious health issue that MAY have started the degenerative process in the spine. Of these serious events, the ones that are most often mentioned are meningitis and Lyme disease.

Plain old "vanilla" blood tests usually reveal "boring" results. You may want to consider getting screened for the mycoplasmas and Borrelia, though most doctors will be resistant to such requests. Why they are is a mystery, given the ample clinical evidence presented internationally (some in this topic).
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Old 06-13-2008, 09:53 AM
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Thank you! It is interesting the correlation between some "triggering event" like stress or another illness and the degeneration.....

Lisa
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Aug 2007 - diagnosed with DDD at C5-6 - herniated disk with mild stenosis at right/central of cord - but pain/occasional numbness mostly on the left side - and down into the leg/foot - which has puzzled doctors - even had a lumbar puncture - but thankfully all clear!
May 2008- after many months of no symptoms and issues- flare up- and new MRI shows moderate stenosis.
L4-5 small annular tear with some DD
Big fan of massages and acupuncture to help with muscle tightness/pain.
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  #28  
Old 06-17-2008, 05:00 PM
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Lisa, well said. Many spine patients do not have a clear picture of the disease factors causing their pain. And still others don't long after surgery -- as this recent abstract illustrates. Here, we see no less than THREE pathological conditions contributing to the poor patient's problem (IMHO, all bacterial; some are gram negative bugs).

This is sad to read, but may be progress in terms of focusing on the pathology of disease. Can you find the three!?

Once again, the US medical system is being outdone by countries who focus on the cause of disease. Most of these "diagnostic" studies are published from overseas. It really gets me mad!
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Delayed spinal infection after laminectomy in a patient with rheumatoid arthritis interruptedly exposed to anti-tumor necrosis factor alpha agents.

Mori S, Tomita Y, Horikawa T, Cho I, Sugimoto M. --- Clinical Research Center for Rheumatic Disease and Department of Rheumatology, Kumamoto Saishunsou National Hospital, 2659 Suya, Kohshi, 861-1196, Japan, moris (at) saisyunsou1.hosp.go.jp.

We report a case of spondylodiscitis caused by Staphylococcus aureus 8 months after laminectomy of the lumbar spine, occurring in a rheumatoid arthritis (RA) patient interruptedly treated with anti-tumor necrosis alpha (TNFalpha) agents. The patient had suffered from seropositive RA for 2 years. An intravenous infusion (200 mg) of infliximab, a chimeric antibody against human TNFalpha, was introduced; however, due to Pneumocystis jiroveci pneumonia, this therapy was withdrawn. Four months later, the patient underwent an L3-L4 and L4-L5 laminectomy for spinal stenosis.

Two months after surgery, we started treatment with 25 mg of etanercept, a soluble humanized TNF receptor dimer, subcutaneously twice a week. At that time, wound healing was satisfactory and no evidence of infection was obtained. Eight months after surgery, septic spondylodiscitis of the lumbar spine occurred.

To the best of our knowledge, this is the first case in the literature to show a delayed type of postoperative infection as a complication of non-instrumented orthopedic surgical procedures. Despite interruption of anti-TNFalpha therapy before surgery, patients may remain at risk of developing postoperative infections.
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  #29  
Old 06-18-2008, 07:31 AM
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Interesting - thanks for sharing that info.

Ok - here is what I see as the 3:

Pneumocystis jiroveci pneumonia
Staphylococcus aureus
rheumatoid arthritis

There were a few other "fancy" words that may also be contributing factors!
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Aug 2007 - diagnosed with DDD at C5-6 - herniated disk with mild stenosis at right/central of cord - but pain/occasional numbness mostly on the left side - and down into the leg/foot - which has puzzled doctors - even had a lumbar puncture - but thankfully all clear!
May 2008- after many months of no symptoms and issues- flare up- and new MRI shows moderate stenosis.
L4-5 small annular tear with some DD
Big fan of massages and acupuncture to help with muscle tightness/pain.
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  #30  
Old 06-18-2008, 09:22 AM
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Rich: just my $0.02 regarding minutiae....Staph is a gram positive bacteria, Pneumoncystis is actually an opportunistic fungus. BUT, many of the other bugs mentioned in the other articles are indeed gram negative bacteria. Gram neg bacteria can be difficult to treat, as many have become resistant to common antibiotics, because of overuse of antibiotics in inappropriate situations (eg. the common cold....it's viral, no point to antibiotics, but some people demand it, and some doctors seem to give in...)
Treating a discitis would generally seem to require long term antibiotics, as the blood supply into the disc itself is not fabulous (I'm speaking from my veterinary experience here...). I've got an appt coming up regarding my shoulder (crikey, it never ends!) and am planning on asking my orthopod about such bacterial theories surrounding DDD, sciatica, blah blah blah. We shall see what she thinks. She is the "medical" orthopedist in the practice I see, vs the "surgical" orthopedist, who is her partner. It's a nice combination of folks, eh?

Susan/ERvet
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New onset left-sided pain Nov 08
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