We report the case of a 34 year old male patient with acute onset and rapidly progressive paraplegia caused by leptomeningeal metastases of an intracranial Glioblastoma Multiforme (GBM), as an illustrative example to enumerate the clinical features and explain the mechanism of spread on the basis of the immunohistochemistry (IHC) of both the primary and secondary tumours. The biopsies of the primary intracranial and the secondary spinal leptomeningeal lesions were subjected to IHC analysis for Glial Fibrillary Acidic Protein (GFAP). Also, 98 additional cases of intracranial GBM with symptomatic leptomeningeal and intramedullary spinal metastases, obtained by review of the literature, are presented here. Mean interval between the identification of spinal metastases and death was 4.5 months. Location of the symptomatic spinal metastases was more frequently leptomeningeal than intramedullary. The case presented in this case report showed high and prominent GFAP expression in both the primary intracranial and secondary leptomeningeal lesions. This runs contrary to the hypothesis proposed by Onda et al and supported by Arita et al. This finding is important as further prospective studies are needed before the pathomechanisms of spinal seeding can be explained on the basis of the tumour’s IHC characteristics alone.

Keywords: Glioblastoma Multiforme; Spinal Metastases; Leptomeningeal Spread; GFAP Expression.