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Neuroborreliosis, also known as Lyme neuroborreliosis (LNB), is a disorder of the central nervous system. A neurological manifestation of Lyme disease, neuroborreliosis is caused by a systemic infection of spirochetes of the genus Borrelia.[1] Symptoms of the disease include erythema migrans and flu-like symptoms.[2] The microbiological progression of the disease is similar to that of neurosyphilis, another spirochetal infection.[3]

Signs and symptoms[edit]

Neuroborreliosis is often preceded by the typical symptoms of Lyme disease, which include erythema migrans and flu-like symptoms such as fever and muscle aches. Neurological symptoms of neuroborreliosis include [[lymphatic meningoradiculitis]], cranial nerve abnormalities, and altered mental status. Sensory findings may also be present. Rarely, a progressive form of encephalomyelitis may occur. In children, symptoms of neuroborreliosis include headache, sleep disturbance, and symptoms associated with increased intracranial pressure, such as papilledema, can occur. Less common childhood symptoms can include meningitis, myelitis, ataxia, and chorea. Ocular Lyme disease has also been reported, as has neuroborreliosis affecting the spinal cord, but neither of these findings are common.[4]

Diagnosis[edit]

A number of diseases can produce symptoms similar to those of neuroborreliosis. They include:

Neuroborreliosis with symptoms consistent with amyotrophic lateral sclerosis has been described.[6]

Diagnosis is determined by clinical examination of visible symptoms.[7] Neuroborreliosis can also be diagnosed serologically to confirm clinical examination via western blot, ELISA, and PCR.[8]

Treatment[edit]

In the US, neuroborreliosis is typically treated with intravenous antibiotics which cross the blood–brain barrier, such as penicillins, ceftriaxone, or cefotaxime.[9] One relatively small randomized controlled trial suggested ceftriaxone was more effective than penicillin in the treatment of neuroborreliosis.[10] Small observational studies suggest ceftriaxone is also effective in children.[11] The recommended duration of treatment is 14 to 28 days.[12][13]

Several studies from Europe have suggested oral doxycycline is equally as effective as intravenous ceftriaxone in treating neuroborreliosis. Doxycycline has not been widely studied as a treatment in the US, but antibiotic sensitivities of prevailing European and US isolates of Borrelia burgdorferi tend to be identical. However, doxycycline is generally not prescribed to children due to the risk of bone and tooth damage.[9]

Discreditied or doubtful treatments for neuroborreliosis include:

Epidemiology[edit]

Neuroborrelisosis is caused by the Borrelia burgdorferi bacterium and is a late-stage manifestation of Lyme disease, the most common vector-borne disease in the northeastern hemisphere.[14] Subsequently, neuroborreliosis is prevalent in areas of high Lyme disease prevalence in North America and Europe.

See also[edit]

References[edit]

  1. ^ Rupprecht, Tobias A; Koedel, Uwe; Fingerle, Volker; Pfister, Hans-Walter (2008). "The Pathogenesis of Lyme Neuroborreliosis: From Infection to Inflammation". Molecular Medicine. 14 (3–4): 205–12. doi:10.2119/2007-00091.Rupprecht. PMC 2148032. PMID 18097481.
  2. ^ Koedel, Uwe; Fingerle, Volker; Pfister, Hans-Walter (2015-08-01). "Lyme neuroborreliosis-epidemiology, diagnosis and management". Nature Reviews. Neurology. 11 (8): 446–456. doi:10.1038/nrneurol.2015.121. ISSN 1759-4766. PMID 26215621. S2CID 13694627.
  3. ^ Miklossy, Judith; Kasas, Sandor; Zurn, Anne D; McCall, Sherman; Yu, Sheng; McGeer, Patrick L (2008). "Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis". Journal of Neuroinflammation. 5 (1): 40. doi:10.1186/1742-2094-5-40. PMC 2564911. PMID 18817547.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Hildenbrand, P.; Craven, D.E.; Jones, R.; Nemeskal, P. (2009). "Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis". American Journal of Neuroradiology. 30 (6): 1079–87. doi:10.3174/ajnr.A1579. PMC 7051319. PMID 19346313.
  5. ^ Lyme Disease at eMedicine
  6. ^ Hänsel, Y.; Ackerl, M.; Stanek, G (1994). "ALS-like sequelae in chronic neuroborreliosis". Wiener medizinische Wochenschrift (1946). 145 (7–8): 186–188. PMID 7610670.
  7. ^ Meyerhoff JO, Zaidman GW and Steele RW for Medscape Drugs & Diseases, Eds. Diamond HS et al. Lyme Disease Differential Diagnoses: Diagnostic Considerations Updated: Mar 14, 2016
  8. ^ CDC Two-step Laboratory Testing Process Page last reviewed: March 4, 2015. Page last updated: March 26, 2015
  9. ^ a b Halperin, John J. (June 2008). "Nervous System Lyme Disease". Infectious Disease Clinics of North America. 22 (2): 261–74, vi. doi:10.1016/j.idc.2007.12.009. PMID 18452800.
  10. ^ Dattwyler RJ, Halperin JJ, Volkman DJ, Luft BJ (May 1988). "Treatment of late Lyme borreliosis--randomised comparison of ceftriaxone and penicillin". Lancet. 1 (8596): 1191–4. doi:10.1016/s0140-6736(88)92011-9. PMID 2897008. S2CID 33352690.
  11. ^ Bloom, Bradley J.; Wyckoff, Patricia M.; Meissner, H. Cody; Steere, Allen C. (March 1998). "Neurocognitive abnormalities in children after classic manifestations of Lyme disease". The Pediatric Infectious Disease Journal. 17 (3): 189–96. doi:10.1097/00006454-199803000-00004. PMID 9535244.
  12. ^ Wormser, G. P.; Dattwyler, R. J.; Shapiro, E. D.; Halperin, J. J.; Steere, A. C.; Klempner, M. S.; Krause, P. J.; Bakken, J. S.; Strle, F.; Stanek, G.; Bockenstedt, L.; Fish, D.; Dumler, J. S.; Nadelman, R. B. (November 2006). "The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America". Clinical Infectious Diseases. 43 (9): 1089–134. doi:10.1086/508667. PMID 17029130. S2CID 4824991.
  13. ^ Halperin, J. J.; Shapiro, E. D.; Logigian, E.; Belman, A. L.; Dotevall, L.; Wormser, G. P.; Krupp, L.; Gronseth, G.; Bever, C. T. (July 2007). "Practice Parameter: Treatment of nervous system Lyme disease (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 69 (1): 91–102. doi:10.1212/01.wnl.0000265517.66976.28. PMID 17522387. S2CID 959269.
  14. ^ Koedel, Uwe; Fingerle, Volker; Pfister, Hans-Walter (2015-08-01). "Lyme neuroborreliosis-epidemiology, diagnosis and management". Nature Reviews. Neurology. 11 (8): 446–456. doi:10.1038/nrneurol.2015.121. ISSN 1759-4766. PMID 26215621. S2CID 13694627.

Category:Lyme disease




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Redhood1/sandbox

Lymphocytic meningoradiculitis[edit]

Lymphocytic meningoradiculitis, also known as Bannwarth syndrome, is a neurological disease characterized as intense nerve pain radiating from the spine. The disease is caused by an infection of Borrelia burgdorferi, a tick-borne spirochete bacteria also responsible for causing Lyme disease.


Signs and symptoms[edit]

Lymphocytic meningoradiculitis is characterized by an intense spinal pain in the lumbar and cervical regions, radiating to the extremities. Symptoms may include facial paralysis, abducens palsy, anorexia, tiredness, headache, double vision, paraesthesia, and erythema migrans.

History[edit]

The disease was first reported in 1941 by German neurologist, Alfred Bannwarth.[1] Bannwarth described the main symptoms as intense radicular pain, facial palsy, severe headaches, and vomiting. A common feature he observed in his infected patients patients was an abnormal increase of lymphocytes in their cerebrospinal fluid (CSF).



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Alfred Bannwarth[edit]

Alfred Bannwarth
Born1903
Munich, Germany
Died1969
NationalityGerman
Known forBannwarth's syndrome

Alfred Bannwarth (1903 – 1970) was a German neurologist who is credited for first reporting lymphocytic meningoradiculitis.[2]


Biography[edit]

Early life and education[edit]

After first studying music, Bannwarth studied medicine graduated in Munich, Germany and later became assistant to German neurologist Max Nonne in Hamburg.[3]

Military service[edit]

Bannwarth enlisted as a military doctor in the German military in 1945. During his service, he was stationed in the valley of Lake Tegern where he was captured by American soldiers and held prisoner until June 1946.[4]


Related bibliography[edit]

  • Chronische lymphocytäre Meningitis, entzündliche Polyneuritis und "Rheumatismus". Ein beitrag zum Problem "Allergie und Nervensystem". Archiv für Psychiatrie und Nervenkrankheiten, Berlin, 1941, 113: 284-376.
  • Zur Klinik und Pathogenese der "chronischen lymphocytären Meningitis". Archiv für Psychiatrie und Nervenkrankheiten, Berlin, 1944, 117: 161-185, 682-716.

External links[edit]



Category:Lyme disease researchers Category:German neurologists Category:1903 births Category:1970 deaths Category:20th-century physicians

  1. ^ Cite error: The named reference Rowland2001 was invoked but never defined (see the help page).
  2. ^ Hippius, Hanns; Möller, Hans-Jürgen; Neundörfer-Kohl, Gabriele (2007-12-31). The University Department of Psychiatry in Munich: From Kraepelin and his predecessors to molecular psychiatry. Springer Science & Business Media. ISBN 9783540740179.
  3. ^ Hippius, Hanns; Möller, Hans-Jürgen; Neundörfer-Kohl, Gabriele (2007-12-31). The University Department of Psychiatry in Munich: From Kraepelin and his predecessors to molecular psychiatry. Springer Science & Business Media. ISBN 9783540740179.
  4. ^ Hippius, Hanns; Möller, Hans-Jürgen; Neundörfer-Kohl, Gabriele (2007-12-31). The University Department of Psychiatry in Munich: From Kraepelin and his predecessors to molecular psychiatry. Springer Science & Business Media. ISBN 9783540740179.
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