It is well-known that viral infections can transfer from the bloodstream to the central nervous system (CNS) by multiple mechanisms with associated secondary inflammation and demyelination. Though uncommon, prior cases of extrapulmonary manifestations of Respiratory Syncytial Virus (RSV) have been reported, including CNS involvement. It is postulated that RSV travels to the CNS via the hematogenous route from the lungs. The following case describes a patient with a viral prodrome, absent respiratory symptoms, followed by acute onset transient neurologic symptoms in the setting of RSV infection.

Case presentation: 

55 year old right handed woman with history of osteoarthritis presented with acute onset disorientation, aphasia, right arm and hand weakness/numbness, and gait instability. This was preceded by 10 days of new onset headaches, neck pain/stiffness and myalgias. The patient had no associated respiratory symptoms, seizures, or fevers. Brain MRI revealed a diffusion restricted lesion involving the splenium of the corpus callosum (SCC), mild associated FLAIR changes, without contrast enhancement. CSF studies showed a lymphocytic predominant pleocytosis at 1100 cells and elevated protein 149. There were no oligoclonal bands. CSF paraneoplastic and meningitis/encephalitis panels were negative. Extensive screen including: HIV, VDRL, Lyme, HSV, VZV, CMV, cryptococcus, ANA, ACE, ESR and CRP were unremarkable. She had no vascular risk factors or metabolic derangements. Respiratory Viral Panel resulted positive for RSV. Her neurologic symptoms resolved spontaneously after approximately one hour and there was complete resolution of SCC lesion upon repeat of brain MRI at 6 months. 

Reversible lesions of the SCC are rare and the causes varied.  The corpus callosum is a highly myelinated tract and lesions in this region are commonly demyelinating and less commonly ischemic. RSV evaluation should be considered in cases involving a lesion of the SCC with an associated viral prodrome and negative CSF and serology.