Meningovascular syphilis is the most prevalent form of neurosyphilis. The meningeal compromise begins during the secondary period of the disease and the CSF usually shows inflammatory signs with presence of lymphocytes and increase of gammaglobulins. The VDRL in CSF is highly specific. The inflammatory phenomenon compromises the cerebral and spinal arteries. We analyzed a very singular case of meningovascular syphilis of the spinal cord in 63 year-old men that expressed a left crural monoplegia associated to urinary retention and contralateral sensitive level, preceded of left flank pain (spinal cord angina) that fulfilled the diagnosis criteria of meningovascular syphilis. The MRI of the spinal cord showed enhanced antero-lateral segmental lesion at D7-D8 and cerebral MRI corroborated the presence of asymptomatic syphilitic arteritis with injuries of both thalamus. The patient was treated with endovenous penicillin G and metilprednisolona that showed significant improvement. We conclude that these manifestations of the neurosyphilis, although rare, are still a reality especially in non treated patients.Cumplía con los criterios diagnósticos de sífilis meningovascular. La RM de la médula espinal mostró una lesión segmentaria en la zona antero-lateral izquierda en D7-D8 y la RM cerebral corroboró la presencia de una arteritis sifilítica con lesiones asintomática en ambos tálamos. Fue tratado con penicilina G endovenosa y metilprednisolona que lo mejoraron significativamente. Se concluye que estas manifestaciones de neurolúes en la médula espinal, aunque raras, siguen vigentes especialmente en paciente no tratados.Palabras clave: Neurosífilis, Sífilis meningovascular, Infarto de la médula espinal.
They may exhibit increased anti-GQ1b antibodies in Miller Fisher syndrome, Guillain-Barre syndrome with ophthalmoplegia, Bickerstaff Rhombencephalitis, and Acute Ophthalmoplegia without ataxia , the so called "anti-GQ1b syndromes". We report a 72 years old man who was admitted because of diplopia, acute onset ophthalmoplegia and retro-ocular pain. He had a similar episode fi ve years ago, fully recovered. At admission he showed complete bilateral ophthalmoplegia without ptosis, miosis and slight enophthalmos of the right eye. Preserved muscle strength, deep tendon arefl exia, without sensory or cerebellar commitment. CSF and electromyography were normal. Brain MRI showed uptake and T2 hyperintensity of the third and sixth cranial nerves. Spinal cord MRI showed no change in the spinal roots. Serum anti-GQ1b increase of 46.2 / 25. He improved without treatment. Thirty days later, paresis was only the sixth pair. The anti-GQ1b is a marker that identifi es neuropathies with oculomotor commitment. The acute ophthalmoplegia without ataxia have normal refl ex, 30% had arefl exia. There are only Guillain-Barré and Miller-Fisher syndromes recurrent case reports with anti-GQ1b. It would be the fi rst case of recurrent anti-GQ1b-positive acute ophthalmoplegia without ataxia.
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