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*Neurosyphilis is now most common in patients with [[HIV]] infection. Reports of neurosyphilis in HIV-infected persons are similar to cases reported before the HIV [[pandemic]]. The precise extent and significance of neurologic involvement in HIV-infected patients with syphilis, reflected by either laboratory or clinical criteria, have not been well characterized. Furthermore, the alteration of host [[immunosuppression]] by [[antiretroviral drug|antiretroviral therapy]] in recent years has further complicated such characterization.
*Neurosyphilis is now most common in patients with [[HIV]] infection. Reports of neurosyphilis in HIV-infected persons are similar to cases reported before the HIV [[pandemic]]. The precise extent and significance of neurologic involvement in HIV-infected patients with syphilis, reflected by either laboratory or clinical criteria, have not been well characterized. Furthermore, the alteration of host [[immunosuppression]] by [[antiretroviral drug|antiretroviral therapy]] in recent years has further complicated such characterization.


==Clinical presentation==
==Clinical presentation: Four clinical types==
*Approximately 35% to 40% of persons with secondary syphilis have [[asymptomatic]] [[central nervous system]] (CNS) involvement, as demonstrated by any of these on [[cerebrospinal fluid]] (CSF) examination:
:*An abnormal leukocyte cell count, protein level, or glucose level
:*Demonstrated reactivity to Venereal Disease Research Laboratory ([[VDRL]]) antibody test
 
==Four clinical types==
*The late forms of neurosyphilis (tabes dorsalis and general paresis) are seen much less frequently since the advent of antibiotics.  
*The late forms of neurosyphilis (tabes dorsalis and general paresis) are seen much less frequently since the advent of antibiotics.  
*The most common manifestations today are asymptomatic or symptomatic meningitis.  
*The most common manifestations today are asymptomatic or symptomatic meningitis.  
Line 82: Line 77:
==Diagnosis==
==Diagnosis==
*Clinical signs of neurosyphilis (i.e., cranial nerve dysfunction, [[meningitis]], [[stroke]], [[altered mental status|acute or chronic altered mental status]], loss of vibration sense, and auditory or ophthalmic abnormalities) warrant further investigation and treatment for neurosyphilis.  
*Clinical signs of neurosyphilis (i.e., cranial nerve dysfunction, [[meningitis]], [[stroke]], [[altered mental status|acute or chronic altered mental status]], loss of vibration sense, and auditory or ophthalmic abnormalities) warrant further investigation and treatment for neurosyphilis.  
*Approximately 35% to 40% of persons with secondary syphilis have [[asymptomatic]] [[central nervous system]] (CNS) involvement, as demonstrated by any of these on [[cerebrospinal fluid]] (CSF) examination:
:*An abnormal leukocyte cell count, protein level, or glucose level
:*Demonstrated reactivity to Venereal Disease Research Laboratory ([[VDRL]]) antibody test


*Laboratory testing is helpful in supporting the diagnosis of neurosyphilis; however, no single test can be used to diagnose neurosyphilis in all instances.
*Laboratory testing is helpful in supporting the diagnosis of neurosyphilis; however, no single test can be used to diagnose neurosyphilis in all instances.

Revision as of 16:15, 16 February 2012

For patient information on Neurosyphilis, click here

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Overview

  • Neurosyphilis may occur at any stage of syphilis.
  • Before the advent of antibiotics, it was typically seen in 25-35% of patients with syphilis.
  • Neurosyphilis is now most common in patients with HIV infection. Reports of neurosyphilis in HIV-infected persons are similar to cases reported before the HIV pandemic. The precise extent and significance of neurologic involvement in HIV-infected patients with syphilis, reflected by either laboratory or clinical criteria, have not been well characterized. Furthermore, the alteration of host immunosuppression by antiretroviral therapy in recent years has further complicated such characterization.

Clinical presentation: Four clinical types

  • The late forms of neurosyphilis (tabes dorsalis and general paresis) are seen much less frequently since the advent of antibiotics.
  • The most common manifestations today are asymptomatic or symptomatic meningitis.
1. Asymptomatic meningitis
  • Asymptomatic neurosyphilis usually has no signs or symptoms and is diagnosed exclusively with the presence or absence of CSF abnormalities notably pleocytosis, elevated protein, decreased glucose.
2. Symptomatic meningitis
  • develops within 6-months to several years of primary infection
  • typical meningitis symptoms: headache, nausea, vomiting, photophobia
  • Acute syphilitic meningitis usually occurs within the first year of infection; 10% of cases are diagnosed at the time of the secondary rash.
  • Patients present with headache, meningeal irritation, and cranial nerve abnormalities, especially the optic nerve, facial nerve, and the vestibulocochlear nerve.
  • Rarely, it affects the spine instead of the brain, causing focal muscle weakness or sensory loss.
3. Meningovascular syphilis
  • Meningovascular syphilis occurs a few months to 10 years (average, 7 years) after the primary syphilis infection.
  • Meningovascular syphilis can be associated with prodromal symptoms lasting weeks to months before focal deficits are identifiable.
  • Prodromal symptoms include:
  • The focal deficits initially are intermittent or progress slowly over a few days.
  • However, it can also present as an infectious arteritis and cause an ischemic stroke, an outcome more commonly seen in younger patients.
  • Angiography may be able to demonstrate areas of narrowing in the blood vessels or total occlusion.
4. Parenchymatous neurosyphilis
  • General paresis[1], otherwise known as general paresis of the insane, is a severe manifestation of neurosyphilis.
  • It is a chronic dementia which ultimately results in death in as little as 2-3 years.
  • Patients generally have progressive personality changes, memory loss, and poor judgment.
  • Imaging of the brain usually shows atrophy.

Diagnosis

  • An abnormal leukocyte cell count, protein level, or glucose level
  • Demonstrated reactivity to Venereal Disease Research Laboratory (VDRL) antibody test
  • Laboratory testing is helpful in supporting the diagnosis of neurosyphilis; however, no single test can be used to diagnose neurosyphilis in all instances.

CSF analysis

  • Diagnosed by finding high numbers of leukocytes in the CSF or abnormally high protein concentration in the setting of syphilis infection.
  • VDRL in cerebrospinal fluid (CSF-VDRL), which is highly specific but insensitive, is the standard serologic test for CSF. Although some advocate using the FTA-ABS test to improve sensitivity.
  • When reactive in the absence of substantial contamination of CSF with blood, it is considered diagnostic of neurosyphilis; however in early syphilis, it can be of unknown prognostic significance.[2]
  • Most other tests are both insensitive and nonspecific and must be interpreted in relation to other test results and the clinical assessment. Therefore, the laboratory diagnosis of neurosyphilis usually depends on various combinations of reactive serologic test results, CSF cell count or protein, and a reactive CSF-VDRL with or without clinical manifestations.

HIV Co-infection

  • There is anecdotal evidence that the incidence of neurosyphilis is higher in HIV patients, and some have recommended that all HIV-positive patients with syphilis should have a lumbar puncture to look for asymptomatic neurosyphilis.[3]
  • Among persons with HIV infection, the CSF leukocyte count usually is elevated (>5 white blood cell count [WBC]/mm3); using a higher cutoff (>20 WBC/ mm3) might improve the specificity of neurosyphilis diagnosis.[4]

Related chapters

Resources

References

  1. Richard B. Jamess, MD, PhD (2002). "Syphilis- Sexually Transmitted Infections, 2006". Sexually transmitted diseases treatment guidelines. External link in |title= (help)
  2. Lukehart SA, Hook EW, Baker-Zander SA, Collier AC, Critchlow CW, Handsfield HH (1988). "Invasion of the central nervous system by Treponema pallidum: implications for diagnosis and treatment". Annals of Internal Medicine. 109 (11): 855–62. PMID 3056164. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  3. Walter T, Lebouche B, Miailhes P; et al. (2006). "Symptomatic relapse of neurologic syphilis after benzathine penicillin G therapy for primary or secondary syphilis in HIV-infected patients". Clin Infect Dis. 43 (6): 787–90. PMID 16912958.
  4. Marra CM, Maxwell CL, Smith SL, Lukehart SA, Rompalo AM, Eaton M, Stoner BP, Augenbraun M, Barker DE, Corbett JJ, Zajackowski M, Raines C, Nerad J, Kee R, Barnett SH (2004). "Cerebrospinal fluid abnormalities in patients with syphilis: association with clinical and laboratory features". The Journal of Infectious Diseases. 189 (3): 369–76. doi:10.1086/381227. PMID 14745693. Retrieved 2012-02-16. Unknown parameter |month= ignored (help)
  5. Jaffe HW, Larsen SA, Peters M, Jove DF, Lopez B, Schroeter AL (1978). "Tests for treponemal antibody in CSF". Archives of Internal Medicine. 138 (2): 252–5. PMID 343742. Retrieved 2012-02-16. Unknown parameter |month= ignored (help)

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