ABSTRACT
Nevin first coined the term ‘‘gliomatosis cerebri’’ (GC) in 1938; he described a diffuse and infiltrative tumor-causing enlargement of cerebral structures without distortion of underlying tissue (1). The first ante mortem diagnosis was made in 1987 (2). The neuronal architecture is preserved in GC and it differs from multifocal gliomas by the lack of detectable connection between the tumors, lack of necrosis, lack of edema with mass effect, and differing enhancement patterns (3). The World Health Organization (WHO) classifies GC as a highly infiltrative neoplasm of the brain (WHO grade III), involving at least two lobes (often bilaterally), by astrocytes, oligodendroglial cells, or a mixture of both (4). GC can be divided into primary and secondary. Two types of GC are distinguished: diffuse infiltration without (type I) or with an associated mass (type II). Secondary GC denotes the remote and contiguous infiltration of tumor cells in a patient with a previously diagnosed glioma (5).
