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{{Neurosyphilis}} | {{Neurosyphilis}} | ||
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==Overview== | ==Overview== | ||
Neurosyphilis refers to a site of infection involving the [[central nervous system]] (CNS). It 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 drug|antiretroviral therapy]] in recent years has further complicated such characterization. | Neurosyphilis refers to a site of infection involving the [[central nervous system]] (CNS). It 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 drug|antiretroviral therapy]] in recent years has further complicated such characterization. | ||
== Historical Perspective == | |||
During the Napeoleonic Wars, General Paresis of the Insane(GPI) first appears to be reported in Paris. In 1836, Marshall Hall an English physician found a patient with loss of postural control in darkness caused by severely compromised [[proprioception]], but He did not develop more information about it. In 1840, [[Moritz Heinrich Romberg]], a german physician was the first who discovered [[Tabes Dorsalis|tabes dorsalis]] which is the most prominent manifestation of neurosyphilis. He described excessive drinking and increase [[sexual activity]] may be the causes of tabes dorsalis. He named the disease as [[Locomotor ataxia|progressive locomotor ataxia]]. He was unable to find the relation between [[syphilis]] and tabes doesalis. In 1858, [[Guillaume Duchenne]] a French [[neurologist]] for the first time described the association between [[syphilis]] and neurosyphilis .In 1875, Jean-Alfred Fournier, a French [[dermatologist]] conclusively described the [[syphilis]] as the main cause of tabes dorsalis. In 1888, Sir William R. Gowers a British [[neurologist]] gave accurate details of the modern [[Romberg's test]]. | |||
== Classification == | |||
The forms of presentation of neurosyphilis can be grouped in two categories: early ([[asymptomatic]] which is the most common form, [[Meninges|meningeal]]<nowiki/>and meningovascular neurosyphilis and late (progressive general paralysis and [[Tabes Dorsalis|tabes dorsalis]]). Other less important forms are [[Gumma (pathology)|gummas]], ocular forms of neurosyphilis and syphilitic [[amyotrophy]] or hypoacusis | |||
==Pathophysiology== | ==Pathophysiology== | ||
Neurosyphilis is caused | Neurosyphilis is caused by [[Treponema pallidum]], the bacteria that cause [[syphilis]]. It usually occurs about 10 - 20 years after a person is first infected with [[syphilis]]. Not everyone who has [[syphilis]] will develop this complication. [[Treponema pallidum|''Treponema pallidum'']] is usually transmitted via direct contact with the infected lesion ([[sexual contact]]) or [[blood transfusion]] (rare). The [[incubation period]] varies with the size of innoculum (9-90 days). Following transmission, [[Treponema pallidum|''Treponema pallidum'']] uses the intact or abraded [[mucous membrane]] to enter the body. It then disseminates to the [[lymphatics]] and blood stream to gain access to any organ of the body. Syphilis uses [[fibronectin]] molecules to attach to the [[endothelial]] surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing [[vasculitis]] ([[endarteritis obliterans]]). Organism has slow replication rate (30-33 hrs) and evades the initial host [[immune response]]. It may seed to different organs of the body especially the [[cardiovascular system]] and [[central nervous system]] resulting in tertiary [[syphilis]]. Different stages of [[syphilis]] results from the interaction between the [[antigen]] and the host immune response. The initial infection in primary [[syphilis]] is limited due to [[Th1 response]] and lack of the [[antibody]]<nowiki/>response. It is speculated that there is a shift from Th1 to [[Th2 response]] during [[secondary syphilis]]. [[Cytotoxic T cells]] and an incomplete [[humoral immunity]] response is mainly responsible for persistence of infection and tissue damage in [[tertiary syphilis]]. Ineffective [[Type IV hypersensitivity|type 4 delayed hypersensitivity]] reaction containing [[macrophages]] and sensitized [[T cells]] is mainly responsible for the [[gumma]] formation in various organs. There is no known [[Genetics|genetic]] association of [[syphilis]]. However, [[neurosyphilis]] may be associated with the gene polymorphism for [[IL-10]] production with increased levels seen in the patients with neurosyphilis. In neurosyphilis, the brain tissue and preganglionic portion of the dorsal roots of spinal nerves is infiltrated with [[Lymphocyte|lymphocytes]] and [[plasma cells]], and invasion of [[treponema pallidum]] [[Spirochaete|spirochete]]<nowiki/>s to brain tissue and [[Posterior column|posterior columns]] of the [[spinal cord]] makes them [[Atrophy|atrophic]]. The [[demyelination]] of the [[Axoneme|axones]] of the [[neurons]] is the main cause of symptoms and it affects the [[neurons]]<nowiki/>in the brain, [[Dorsal root ganglion|dorsal root ganglia]] and [[Posterior columns|posterior columns of the spinal cord]]. | ||
==Diagnosis== | ==Diagnosis== | ||
===History and Symptoms=== | ===History and Symptoms=== | ||
Revision as of 00:00, 6 April 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Neurosyphilis refers to a site of infection involving the central nervous system (CNS). It 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.
Historical Perspective
During the Napeoleonic Wars, General Paresis of the Insane(GPI) first appears to be reported in Paris. In 1836, Marshall Hall an English physician found a patient with loss of postural control in darkness caused by severely compromised proprioception, but He did not develop more information about it. In 1840, Moritz Heinrich Romberg, a german physician was the first who discovered tabes dorsalis which is the most prominent manifestation of neurosyphilis. He described excessive drinking and increase sexual activity may be the causes of tabes dorsalis. He named the disease as progressive locomotor ataxia. He was unable to find the relation between syphilis and tabes doesalis. In 1858, Guillaume Duchenne a French neurologist for the first time described the association between syphilis and neurosyphilis .In 1875, Jean-Alfred Fournier, a French dermatologist conclusively described the syphilis as the main cause of tabes dorsalis. In 1888, Sir William R. Gowers a British neurologist gave accurate details of the modern Romberg's test.
Classification
The forms of presentation of neurosyphilis can be grouped in two categories: early (asymptomatic which is the most common form, meningealand meningovascular neurosyphilis and late (progressive general paralysis and tabes dorsalis). Other less important forms are gummas, ocular forms of neurosyphilis and syphilitic amyotrophy or hypoacusis
Pathophysiology
Neurosyphilis is caused by Treponema pallidum, the bacteria that cause syphilis. It usually occurs about 10 - 20 years after a person is first infected with syphilis. Not everyone who has syphilis will develop this complication. Treponema pallidum is usually transmitted via direct contact with the infected lesion (sexual contact) or blood transfusion (rare). The incubation period varies with the size of innoculum (9-90 days). Following transmission, Treponema pallidum uses the intact or abraded mucous membrane to enter the body. It then disseminates to the lymphatics and blood stream to gain access to any organ of the body. Syphilis uses fibronectin molecules to attach to the endothelial surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing vasculitis (endarteritis obliterans). Organism has slow replication rate (30-33 hrs) and evades the initial host immune response. It may seed to different organs of the body especially the cardiovascular system and central nervous system resulting in tertiary syphilis. Different stages of syphilis results from the interaction between the antigen and the host immune response. The initial infection in primary syphilis is limited due to Th1 response and lack of the antibodyresponse. It is speculated that there is a shift from Th1 to Th2 response during secondary syphilis. Cytotoxic T cells and an incomplete humoral immunity response is mainly responsible for persistence of infection and tissue damage in tertiary syphilis. Ineffective type 4 delayed hypersensitivity reaction containing macrophages and sensitized T cells is mainly responsible for the gumma formation in various organs. There is no known genetic association of syphilis. However, neurosyphilis may be associated with the gene polymorphism for IL-10 production with increased levels seen in the patients with neurosyphilis. In neurosyphilis, the brain tissue and preganglionic portion of the dorsal roots of spinal nerves is infiltrated with lymphocytes and plasma cells, and invasion of treponema pallidum spirochetes to brain tissue and posterior columns of the spinal cord makes them atrophic. The demyelination of the axones of the neurons is the main cause of symptoms and it affects the neuronsin the brain, dorsal root ganglia and posterior columns of the spinal cord.
Diagnosis
History and Symptoms
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. Clinical signs of neurosyphilis (i.e., cranial nerve dysfunction, meningitis, stroke, acute or chronic altered mental status, loss of vibration sense, and auditory or ophthalmic abnormalities) warrant further investigation and treatment for neurosyphilis.
Laboratory Findings
Approximately 35% to 40% of persons with secondary syphilis have asymptomatic central nervous system (CNS) involvement, as demonstrated by an abnormal leukocyte cell count, protein level, or glucose level or a demonstrated reactivity to Venereal Disease Research Laboratory (VDRL) antibody test on cerebrospinal fluid (CSF) examination. Laboratory testing is helpful in supporting the diagnosis of neurosyphilis; however, no single test can be used to diagnose neurosyphilis in all instances.
Medical Therapy
CNS involvement can occur during any stage of syphilis. However, CSF laboratory abnormalities are common in persons with early syphilis, even in the absence of clinical neurological findings. No evidence exists to support variation from recommended treatment for early syphilis for patients found to have such abnormalities. If clinical evidence of neurologic involvement is observed (e.g., cognitive dysfunction, motor or sensory deficits, ophthalmic or auditory symptoms, cranial nerve palsies, and symptoms or signs of meningitis), a CSF examination should be performed. Syphilitic uveitis or other ocular manifestations frequently are associated with neurosyphilis and should be managed according to the treatment recommendations for neurosyphilis. Patients who have neurosyphilis or syphilitic eye disease (e.g., uveitis, neuroretinitis, and optic neuritis) should be treated with the recommended regimen for neurosyphilis; those with eye disease should be managed in collaboration with an ophthalmologist. A CSF examination should be performed for all patients with syphilitic eye disease to identify those with abnormalities; patients found to have abnormal CSF test results should be provided follow-up CSF examinations to assess treatment response.
Prevention
Prompt diagnosis and treatment of the original syphilis infection can prevent neurosyphilis.