Superficial Siderosis of Central Nervous System Mimicking Multiple Sclerosis

Papadimas, GK; Rentzos, M; Zouvelou, V; Kilidireas, K; Konstantinopoulou, A; Kokotis, P; Evdokimidis, I

dc.contributor.author	Papadimas, GK	en
dc.contributor.author	Rentzos, M	en
dc.contributor.author	Zouvelou, V	en
dc.contributor.author	Kilidireas, K	en
dc.contributor.author	Konstantinopoulou, A	en
dc.contributor.author	Kokotis, P	en
dc.contributor.author	Evdokimidis, I	en
dc.date.accessioned	2014-03-01T01:58:59Z
dc.date.available	2014-03-01T01:58:59Z
dc.date.issued	2009	en
dc.identifier.issn	1074-7931	en
dc.identifier.uri	https://dspace.lib.ntua.gr/xmlui/handle/123456789/28807
dc.subject	multiple sclerosis	en
dc.subject	oligoclonal hands	en
dc.subject	superficial siderosis	en
dc.subject.classification	Clinical Neurology	en
dc.title	Superficial Siderosis of Central Nervous System Mimicking Multiple Sclerosis	en
heal.type	journalArticle	en
heal.language	English	en
heal.publicationDate	2009	en
heal.abstract	Introduction: Superficial siderosis of the central nervous system is a neurologic disorder mainly characterized by cerebellar involvement, myelopathy, neurosensory hearing loss, and possibly progressive cognitive impairment. Root avulsion due to traumatic plexus injury has been recognized as an extremely rare cause of hemosiderin deposition oil leptomeninges and subpial layers of brain and spinal cord parenchyma. Case Report: A 49-year-old mail presented with progressively evolving ataxia and spastic paraparesis. CSF oligoclonal bands were indicative of an underlying inflammatory process and raised the possibility of a demyelinating disorder. However, spinal cord and brain MRI revealed hemosiderin deposition along the entire neuraxis. A rigorous electrophysiologic study confirmed a functional impairment in many different levels of the nervous system. Conclusion: The demonstration of CSF oligoclonal bands in the reported patient implies that inflammation might be involved in the pathogenesis of superficial siderosis. The diagnosis of this newly recognizable entity needs a high clinical suspicion, but further research is needed to fully elucidate the involved mechanisms.	en
heal.publisher	LIPPINCOTT WILLIAMS & WILKINS	en
heal.journalName	NEUROLOGIST	en
dc.identifier.isi	ISI:000266029600008	en
dc.identifier.volume	15	en
dc.identifier.issue	3	en
dc.identifier.spage	153	en
dc.identifier.epage	155	en