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Introduction
Syphilis is a sexually transmitted disease whose pathogen is Treponema pallidum, a gram-negative spirochete. The gateway is the tegument or mucous membranes at the level of minimal lesions (1). From a pathophysiological point of view, the main process triggered by Treponema pallidum infection is an obliteration of terminal arterioles, with inflammatory changes and necrosis. In the central nervous system, infection causes chronic inflammation of the meninges and blood arteries, which over time may be complicated by parenchymal lesions (1).
Early invasion (not necessarily ‘involvement’) of the central nervous system, is thought to occur in numerous (if not most) patients infected with syphilis. Thus, it is not surprising that neurological manifestations of syphilis may occur at any stage of infection (2). While neurosyphilis itself is a complication of syphilis, untreated neurosyphilis may lead to devastating neurological sequelae, including permanent paralysis, dementia and death. Treatment should be initiated immediately, and certain complications may be reversible. The success of therapy has an inverse relationship with the duration of untreated infection (3). As there is no single highly sensitive and specific diagnostic test, it is based on clinical manifestations and cerebrospinal fluid (CSF) abnormalities (4).
The present article reviews the clinical manifestations, diagnostic process and first-line treatment of neurosyphilis, with a focus on the neurological symptoms, important to the clinician.
Case reports
Case 1
The first case was a 28-year-old male, with no personal pathological history, who presented at the Neurology Clinic of ‘Sf. Ap Andrei’ Emergency County Clinical Hospital (Constanta, Romania) in July 2022 due to Jacksonian epileptic episodes in the left arm, which had begun ~2 weeks previously, and the patient was under a treatment recommended by the neurologist with Levetiracetam (500 mg every 12 h). The patient was hospitalized at the Neurology Department of the Emergency Clinical Hospital (Constanta, Romania) for 5 days.
At the time of admission, an objective neurological examination revealed Jacksonian epileptic seizures in the left upper limb without any other neurological symptoms. A native brain MRI and magnetic resonance angiography with venous time were performed (which indicated a cortical, parietal, well-defined lesion that had not absorbed the gadolinium-based contrast substance; (Fig. 1) and an electroencephalogram was performed (which indicated a microvoltage pathway of 11.5 c/sec, modulated in spindles, without graphs...