University of Rochester Medical Center
SearchDirectoryNewsEventsStrong HealthURMC Home

Images below require Macromedia's Flash Player to view

Previous Case Next Case

Neuroradiology Case of the Week

Case 144

Alisa Johnson, Loris Cedeno, MD, Jeevak Almast, MD,
and PL Westesson MD, DDS, PhD

Clinical Presentation: A 33-year-old female, with past history significant for a resected glioblastoma multiforme and radiation treatment at the age of 5 years old, presents with acute onset seizures and new intracranial mass.

Radiological Findings: CT shows interval development of a mass located in the left insula adjacent to the left lateral ventricle. On non-contrast images, it has increased attenuation (Fig. 1). Post-contrast, it demonstrates enhancement. This lesion has minimal mass effect with no significant surrounding edema (Fig. 2).
     A surgical cavity within the right frontal lobe represents the resection of the prior tumor (Fig. 3). Figure 4 is an axial MRI of the pt almost two years prior to her recurrence. There is no evidence of new tumor but the post operative and radiation changes are noted.

Figure 1: Axial CT noncontrast.

Figure 2: Axial CT with Gd.

Figure 3: Axial CT noncontrast. Figure 4: Axial T1WI.

Differential diagnosis: Differential diagnosis for the GBM includes other neoplasms like anaplastic astrocytomas or metastasis. Non-neoplastic ring enhancing masses include an abscess and “tumefactive” demyelination. However, “tumefactive” demyelination is usually horse-shoe shaped with an incomplete enhancing ring, open towards the cortex.

Diagnosis: Recurrent Glioblastoma multiforme

Clinical Discussion: Glioblastoma multiformes (GBM), also known as grade IV astrocytomas, are the most common and most malignant adult primary brain neoplasm, representing 15-20% of primary CNS neoplasms. They usually occur in patients > 50 years old but can occur at any age. GBMs represent approximately half of all astrocytomas [1].
     Clinically the presentation of GBM varies depending on the location and size of the lesion. GBM can invade and compress brain parenchyma and cause increase of intracranial pressure through restricting cerebrospinal fluid outflow, resulting in hydrocephalus. Typically GBM present with seizures and hemiparesis, but depending on the variables mentioned above they can also present with other focal neurologic deficits or stroke-like syndromes [1].
     GBMs have a poor prognosis with a median postoperative survival of 12 months and a 5 year recurrence-free survival rate of <5% [2]. This case study shows an exceptional outcome for someone who was diagnosed with a GBM. The radiation treatment she had when she was five may have played a role in the recurrence of a GBM on the contralateral side; however, she has done exceptionally well to have survived a GBM for 27 years.

Neuroimaging Discussion: The typical location for a GBM is in the deep cerebral white matter especially in the frontal or temporal lobes. Bihemispheric tumors that extend through corpus callosum are common resulting in the “butterfly” type GBM. Classic findings in GBM are nodular rim of enhancement with a large amount of surrounding edema and mass effect. CT scans typically show low density regions that reflect necrosis or cyst formation in 95% of cases [3]. Peripheral edema is common and surrounds the tumor, extending into the white matter tracts. Hemorrhage of different ages is common but calcifications are uncommon. Following contrast administration, CT often shows a thick irregular rim enhancement.
     
MRI T1WI demonstrates a mass that is hypointense with a poorly delimitated mixed signal mass with cyst formation or necrosis and a thick irregular wall. GMB are often very vascular tumor which will demonstrate flow voids and hemorrhages of different ages. While a hyperintense mass is seen on T2WI and FLAIR usually with a striking amount of edema. Although, the edema is hyperintense and not easily distinguished from the tumor it is the best measure of the tumor margins. It is important to note that isolated tumor cells may extend beyond the T2WI hyperintense region into what looks like normal brain parenchyma.

References:

  1. Osborn AG. Diagnostic Imaging: Brain. 1st ed. Amirsys Inc: Altona, 2004.
  2. Grossman, R., Yousem, D. Neuroradiology, The Requisites. 2nd ed. Elsevier Inc. Philadelphia, 2003.
  3. Castillo, M. The Core Curriculum: Neuroradiology. Lippincott Williams & Wilkins, Philadelphia: 2002.
Next Case