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Neurosyphilis

Tertiary stage of syphilis that occurs in about 10% of patients untreated for syphilis.

Neurosyphilis can occur at any stage of infection, within six weeks of infection between 25 and 60% of patients have evidence of CNS dissemination, although only 5% develop symptoms.

Early neurosyphilis usually presents is meningitis and  neurosyphilis  can result in generalized paresis or tabes dorsalis.

General paresis occurs in 2 to 5% of patients who remained untreated after 20 to 30 years NTBs the cells develops in 2 to 9% of patients who are untreated after 3 to 50 years.

Neurologic involvement occurs during all stages of syphilis.

Certain treponemal tapes have increased propensity to invade the CNS.

CNS invasion by treponemes is accompanied by abnormal CSF findings in up to 50% of the persons after early infection even in the absence of clinical features.

CSF abnormalities typically resolved after recommended therapy.

It is a result of infection has the nervous system by Treponema palladium,

Major forms include meningovascular, paretic and tabes dorsalis.

And uncommon process now, but 3.5% of patients with clinical or ophthalmologic features of syphilis and neurosyphilis on the basis of CSF findings.

Rates of neurosyphilis range from 0.47-2.1 cases per hundred thousand population.

Half of patients with early syphilis have been coinfected with the HIV virus, and neurosyphilis is estimated to occur is twice as many persons with coinfection face persons without HIV infections.

Early neurosyphilis is characterized by asymptomatic meningitis, established only by a cellular reaction in the CSF.

Early neurosyphilis, however, can be symptomatic with headache, meningismus cranial nerve palsy, blindness or deafness.

Meningeal vascular syphilis involves vasculitis of small and medium size arteries in the CNS and can cause strokes and myelopathy.

Early neurosyphilis includes meningitis, with cranial nerve abnormalities.

Late stage neurologic manifestations are either meningeal vascular or parenchymal.

Late symptomatic neurosyphilis develops decades after the primary infection.

Late neurosyphilis manifests as general paresis and tabes dorsalis.

Tertiary, late, stage disease may manifest as hemiplegia, aphasia and seizures.

Spinal cord blood vessels may be involved with meningomyelitis and spinal vascular syphilis.

Parenchymal forms of disease-general paresis and tabes dorsalis tend to occur greater than 15 years after infection.

General paresis manifestations include irritability,cognitive and memory impairments, followed by emotional lability delusions and paranoia.

Tabes dorsalis symptoms include lightning pains, ataxia, bladder disturbances, visceral crises, and rectal incontinence.

General paresis and tabes dorsalis are result of chronic meningeal reaction to spirochetal invasion and destruction of adjacent neural tissue, sometimes along with cerbral infarction.

General paresis is associated with frontal temporal dementia, with grandiose delusions, unusual talking and repetitive speech patterns, and if untreated progresses to state of mental and physical dissolution, often with seizures.

General paresis is characterized by psychosis, depression, personality change, possibly nondescript progressive dementia and sometimes flamboyant delusions.

Tabes is characterized by ataxia of gait, with a positive Romberg sign, and in most cases by Argyll Robertson pupils.

Pains in the abdomen and limbs from tabes can mimic emergency disorders.

Neurologic deficits including visual or hearing changes may be subtle.
Ocular and codec neurosyphilis can occur.

Ocular syphilis may affect any part of the eye, but uveitis is the most common presentation.

Laboratory diagnosis is based on abnormal serum and CSF serology tests and elevations of CSF white blood cell count and protein levels, but all tests are imperfect.

Blood in CSF serological testing are classified as non-treponemal (VDRL or rapid plasma reagin (RPR) or treponemal using fluorescent treponemal and a body absorption (FTA-ABS).

It is usually accompanied by CSF pleocytosis, and mildly elevated protein levels.

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