Cerebral vasculitis due to Treponema pallidum infection: MRI and MRA findings.

Abstract

Accepted: 1 July 2003 Published online: 2 October 2003 © Springer-Verlag 2003 Sir, A 44-year-old male was admitted because of recurrent transient ischemic attacks with right-sided hemiparesis. The patient was tested HIV positive 9 months before admission and his infection without an AIDSdefining illness was treated with three different reverse transcriptase inhibitors. In addition, 8 years previously he had suffered from luetic infection and at that time he was treated with tetracyclines. On neurological examination motoric functions of the limbs were unremarkable. Laboratory tests were positive for Treponema pallidum hemagglutinin (TPHA), fluorescent treponemal antibody absorption (FTAABS) IgG and IGM, as well as Venereal Disease Research Laboratory (VDRL). Cerebrospinal fluid (CSF) disclosed elevated protein content with 87.6 mg/100 ml as well as autochthone IgG (14.7 mg/ 100 ml) and IgM (2.0 mg/100 ml) intrathecal production. Cultures for bacteria and other microorganisms, including fungi, were negative. Initial MRI demonstrated small hyperintense lesions in the basal ganglia on T2-weighted as well as on diffusion-weighted images (DWI; b=1000 s/mm2; Fig. 1) typical for subacute lacunar infarctions. The MRA showed bilateral severe stenoses of the distal M1 and proximal M2 segments (Fig. 2). With regard to laboratory and neuroradiological findings, active neurosyphilis with vascular involvement was diagnosed. The patient was treated with i.v. ceftriaxone (2 g/day for 21 days), clopidogrel (75 mg/day), and aspirin (100 mg/day). Up to neurological follow-up 2 months later, there was no further ischemic event. Syphilis remains an important and frequently encountered sexually transmitted disease caused by Treponema pallidum. The central nervous system (CNS) may become involved in any stage of the disease from weeks to years after the initial infection. Neurosyphilis is seen primarily in the tertiary and occasionally in the secondary stage of the disease. Pathological findings of neurosyphilis include acute syphilitic meningitis, meningovascular neurosyphilis, and parenchymatous neurosyphilis [1]. Diagnostic confirmation of neurosyphilis requires a positive FTA test and a positive CSF VDRL test accompanied by CSF pleocytosis and elevated CSF protein levels. The meningovascular form of neurosyphilis is usually associated with a prodromal clinical course of weeks to months before the onset of identifiable vascular syndromes. The most common clinical presentation is an ischemic syndrome in a young adult, involving the middle cerebral artery or less commonly the branches of the basilar artery. Eur Radiol (2004) 14:746–747 DOI 10.1007/s00330-003-2015-4 L E T T E R T O T H E E D I T O R