AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

According to the American Cancer Society, approximately 22,000 malignant tumors of the brain (ie, malignant glioma) and spinal cord will be diagnosed in 2008, constituting 1.3% of all cancers and 2.2% of all cancer-related deaths. Approximately 12,000 cases will occur in males, and 10,000 cases in females.¹

Glioblastomas are the most common adult malignant brain tumors, and 20% of all primary brain neoplasms are glioblastoma multiforme (GBM) tumors.

The 3 major types of brain tumor are astrocytoma, oligodendroglioma, and ependymoma. These are all considered gliomas, tumors that begin in the glial cells, such as astrocytes, oligodendrocytes, and ependymal cells.^{1, 2}

Senator Edward M. Kennedy was diagnosed with a malignant glioma on May 20, 2008, at Massachusetts General Hospital. The diagnosis was made following a seizure, a common presentation in patients with this type of brain tumor.³

Astrocytic tumors represent as many as 75% of primary brain gliomas. They are the most common primary brain tumor in children (posterior fossa predominance, particularly in the brain stem) and adults (mostly supratentorial⁴). They are divided into low grade, intermediate grade (anaplastic astrocytomas), and high grade (glioblastomas). Glioblastoma multiforme (GBM) is the highest-grade form of astrocytoma and makes up about two thirds of all brain astrocytomas, as well as 20% of primary brain neoplasms. Glioblastomas are the most common adult malignant brain tumors.^{5, 6, 7}

Oligodendrogliomas represent approximately 4% of all brain tumors and begin in the oligodendrocytes.

Ependymomas make up about 2% of brain tumors, which originate in the ependymal cells.

The lower-grade gliomas (World Health Organization [WHO] grades I and II) tend to progress to GBM with time.^{8, 9, 10, 11}

Genetic factors include the following^{12, 13}:

• Tumor suppressor gene mutations in TP53
• • In arm 17p
  • Sporadic or part of a familial or inherited cancer syndrome
    • Turcot syndrome
    • Neurofibromatosis I
    • Li-Fraumeni syndrome (This is inherited in an autosomal dominant fashion. Patients have an increased risk for malignancies, particularly soft-tissue sarcomas and breast malignancies. About 10% of patients have brain tumors, mostly gliomas.)
  • Loss of heterozygosity on arm 19q
  • Tumor suppressor gene mutation on arm 3q
  • Loss of heterozygosity on chromosome 10
    • Most common chromosomal abnormality found in GBM
    • Not commonly seen in other tumors (versus TP53 mutations)
    • May be specific for GBM

Related eMedicine topics:
Glioblastoma Multiforme (Neurology)
Glioblastoma Multiforme (Oncology)
Brain Metastasis
Brainstem Gliomas
EEG in Brain Tumors
Astrocytoma, Brain
Brain, Lymphoma

Related Medscape topics:
CME/CE  Multidisciplinary Perspectives on Management of Glioblastoma Multiforme
CME Surgery Insight: The Role of Surgery in the Management of Low-Grade Gliomas
Autocrine Factors That Sustain Glioma Invasion and Paracrine Biology in the Brain Microenvironment
Management of Malignant Glioma: Steady Progress With Multimodal Approaches.
Stem Cell Therapies for Malignant Glioma
Gene Therapy for Glioblastoma
Standard Treatment and Experimental Targeted Drug Therapy for Recurrent Glioblastoma Multiforme.
Angiogenesis Inhibition: The Next Frontier in Multimodal Therapy for Glioblastoma Multiforme

Pathophysiology

The histologic hallmarks of glioblastoma multiforme (GBM) include intense cytologic diversity (multiforme), neovascularity, hemorrhage, areas of necrosis surrounded by neoplastic cell layers in a pseudopalisading array. Within the tumor, different areas may have different histologic appearances; therefore, the possibility of undergrading the tumor exists if a limited biopsy sample is obtained.⁵

Glioblastoma multiforme, or GBM, is a highly infiltrative tumor. For this reason, tumor cells are usually found beyond the margins of an area of abnormal signal intensity on magnetic resonance images (MRIs). CNS metastases are frequent, but extracerebral metastases are rare.

Tumor spreads via white matter tracts, commonly through the corpus callosum (butterfly glioma, main differential diagnosis is lymphoma) and commissures. They may spread to the infratentorial compartment. Other routes of dissemination involve ependymal and leptomeningeal routes and the CSF. These tumors may also cause hematogenous metastasis, and in some cases, they may directly invade the skull. They may be multicentric (no connection) or multifocal (microscopic connections), with multiple separate masses.

Some forms of GBM are considered variants, as follows:

• Giant cell glioblastoma (monstrocellular GBM)
  • Multinucleated giant glial cell histologic features
  • Same imaging findings as those of GBM
  • Prognosis similar to that of classic GBM, although some authors claim that it might be slightly better in this form
• Gliosarcoma
  • About 2-8% of GBMs
  • Mixed gliomatous and sarcomatous elements from dedifferentiation of glioblastomatous cells to a malignant glial-mesenchymal precursor line
  • Intense associated desmoplastic reaction (desmoplastic glioblastomas)
  • Propensity for dural and calvarial invasion
  • Distant metastasis in 15-30% of cases, otherwise prognosis similar to that of GBM
  • Temporal lobe predominance
• Gliomatosis cerebri
  • Diffuse neoplastic astrocytic infiltration with gross architectural preservation, no focal mass
  • Flattened, wide gyri
  • May be diffuse form of GBM (However, this is controversial; hence, the separate WHO classification.)
  • White-matter tract predominance, but gray matter may be affected

Frequency

United States

Glioblastoma multiforme (GBM) represents two thirds of brain astrocytomas, as well as 20% of primary brain neoplasms.

International

No variability in presentation is known to be reported in cases of glioblastoma multiforme outside of the United States.

Mortality/Morbidity

Glioblastoma multiforme represents the worst end of the glioma spectrum, and as such, it has the worst prognosis.^{5, 14}

• Most patients die within 8-18 months of diagnosis.
• Patients whose initial presentation is that of long-standing seizures have a somewhat improved prognosis, and this difference may indicate the transformation of a benign glioma into a glioblastoma.¹⁵ The patients usually die from extension and growth of the primary tumor.

Race

Glioblastoma multiforme affects white patients more often than patients in other racial groups.

Sex

Glioblastoma multiforme has a slight male predilection. In some studies, the male-to-female ratio is reported to be 3:2.

Age

The peak age for the diagnosis of glioblastoma multiforme (GBM) is 50-70 years. However, the age of patients in whom GBM is diagnosed varies widely; this tumor can develop in patients of any age. Gliomatosis cerebri usually affects young or middle-aged patients.^{5, 16, 17}

Anatomy

The most common location for glioblastoma multiforme tumors (GBMs) is the cerebral hemisphere, commonly the deep white-matter regions. Frontal and temporal lobes are more commonly involved. The tumor may also involve the basal ganglia; the cortex may also be involved, although not as frequently. It may also involve the corpus callosum, either by arising in it or by extending to it. Because the tumor spreads via white-matter tracts, it may cross the corpus from one side to the other, in a pattern known as butterfly glioma. In addition, cerebellar and/or spinal GBMs can occur.

Clinical Details

The presentation of glioblastoma multiforme is varied and depends on the location of the tumor and the anatomic structures involved.

Common symptoms include strokelike symptoms, focal strokelike symptoms, focal neurologic deficits, headaches, changes in behavior, frontal lobe involvement, and seizures. Motor seizures include generalized tonic-clonic seizures. Nonmotor seizure activity, such as involvement of the temporal lobe (eg, olfactory hallucinations), may occur. Jacksonian seizures may be noted. Focal seizures may begin in part of an extremity and progress to involve all or part of one side of the body.

Preferred Examination

Although computed tomography (CT) can demonstrate the tumor and associated findings, the modality of choice for the examination of a patient with suspected or confirmed glioblastoma multiforme (GBM) is MRI. Positron emission tomography (PET) is useful after surgical resection to differentiate between recurrent tumor and scar tissue.^{18, 19, 20, 21, 22, 23, 24, 25}

In terms of the imaging appearance and the appearance of a mass in the spectrum from low-grade astrocytoma to GBM, some generalizations can be made (though some exceptions apply):

(1) The incidence of calcification decreases in the spectrum from low-grade astrocytoma to GBM.

(2) The incidence of enhancement increases in the spectrum from low-grade astrocytoma (preserved blood-brain barrier [BBB], low enhancement frequency) to GBM (disrupted BBB).

(3) Hemorrhage, necrosis, mass effect, and edema incidence patterns are the same as those for enhancement.

(4) Unless hemorrhagic changes are present, most tumors are hypointense on T1-weighted MRIs and hyperintense on T2-weighted MRI.

(5) Enhancement on CT scans means enhancement on MRIs.

Limitations of Techniques

CT may cause small tumors to be missed. In addition, it may not depict all multifocal lesions. CSF spread, particularly early spread, may also be difficult to diagnose with CT.

MRI is significantly more sensitive to the presence of tumor, as well as its associated findings, in the inclusion of peritumoral edema. However, as previously noted, tumor usually microscopically extends beyond the visible margins of signal intensity abnormality on MRIs. In addition, after surgery, differentiating between recurrent tumor and scar tissue on the basis of MRI findings alone may be difficult. PET scanning is helpful in this regard.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Tumefaction, brain

RADIOGRAPH

Section 4 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Radiographs are not used in the evaluation of the primary tumor. However, in cases of tumors that invade the calvarium, x-ray studies may demonstrate skull erosion changes. In the uncommon case with distant skeletal metastases, radiographs may demonstrate these as well.

Degree of Confidence

This imaging modality has no usefulness in the diagnosis of the primary tumor, and it is only used in cases of suspected calvarial invasion.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Findings at nonenhanced CT may include the following:

• Heterogeneous poorly marginated mass
• Internal areas of low or fluid attenuation
  • Foci of necrosis
  • Present in as many as 95% of GBMs
• Internal areas of high attenuation
  • Foci of hemorrhage
  • Calcifications rare (more common if GBM is the result of transformation of a low-grade astrocytoma or after therapy)
• Significant mass effect and edema (vasogenic distribution of the edema)

Findings at enhanced CT include significant enhancement with the following features:

• Irregularity and inhomogeneity
• Possible ring enhancement
• Solid enhancement possible, but uncommon
• Little enhancement possible in diffuse forms

With gliomatosis cerebri, CT findings may be normal, or scans can show widespread low-attenuating regions, with no focal mass and no enhancement.

Degree of Confidence

CT results offer a relatively high degree of confidence for the diagnosis of glioblastoma multiforme (GBM). However, some lesions may mimic a GBM (see False Positive/Negatives, below).

False Positives/Negatives

False-positive cases may be due to space-occupying lesions such as brain abscess, infarct with hemorrhagic transformation, and neoplasms of a lower grade than that of glioblastoma multiforme (GBM). In addition, some types of demyelinating lesions (eg, giant multiple sclerosis plaques) may mimic a GBM. The multifocal form of GBM may be indistinguishable from diffuse multiple sclerosis.

MRI

Section 6 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

MRI findings include the following²⁶:

• Heterogeneous mass, generally of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images
• Internal cystic areas
• Necrotic foci
• Internal areas of high signal intensity on T1 (hemorrhagic foci)
• Irregular but intense enhancement after the administration of gadolinium-based contrast material (same pattern as with enhanced CT)
• Internal flow voids (these represent prominent vessels)
• Neovascularity
• Significant peritumoral vasogenic edema
• Significant mass effect
• Metastatic foci
  • Intracerebral metastasis common with GBM
  • Higher sensitivity to these lesions with MRI than with CT
• Gliomatosis cerebri
  • Diffuse white-matter abnormality
  • Signs of increased intracranial pressure, including ventricular compression, subarachnoid space obliteration (differential diagnosis includes normal pressure hydrocephalus)
• Gliosarcoma
  • Sarcomatous element, usually well circumscribed
  • Infiltrative gliomatous element
  • Possibly resembling meningioma
  • Other imaging findings similar to those of GBM

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

MRI has a high degree of confidence in the diagnosis of glioblastoma multiforme. In fact, it has the highest degree of confidence of any imaging modality.

False Positives/Negatives

Some lesions, mainly space-occupying lesions with hemorrhagic components, may mimic glioblastoma multiforme on MRIs. These include abscesses and infarcts.

ULTRASOUND

Section 7 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Ultrasonography has no role in the evaluation of glioblastoma multiforme.

NUCLEAR MEDICINE

Section 8 of 12  

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• Intervention
• Multimedia
• References

Findings

Positron emission tomography (PET) scanning is a useful adjunct to the evaluation of glioblastoma multiforme (GBM), particularly after resection. In this setting, differentiation of residual or recurrent tumor and postoperative edema or scarring is often difficult on MRIs or CT scans. PET with 18-fluorodeoxyglucose (FDG) is useful in cases of active tumor, which shows high metabolic activity and glucose utilization, and in cases of simple postoperative edema or scars, which usually have no increased activity.

Degree of Confidence

In the setting of resection for known tumor, the finding of increased tracer uptake at the surgical site is a reliable indicator of recurrent disease. However, after radiotherapy, increased activity may be seen at the surgical site without tumor recurrence (see False Positives/Negatives below).

False Positives/Negatives

False-positive findings occur after radiation therapy, when active granulation tissue can metabolize FDG, which may limit the sensitivity of the study in this setting. An epileptogenic focus near the surgical site may show increased uptake on PET scanning, particularly if epileptic activity is high.

ANGIOGRAPHY

Section 9 of 12  

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• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Angiographic findings associated with glioblastoma multiforme include the following: hypervascular mass with tumor blush; prominent feeding and draining vessels, as well as arteriovenous shunting (this may mimic an arteriovenous malformation); aberrant vessels and vascular pooling and stasis (common); and mass effect, which is seen as displacement of vessels.

Degree of Confidence

Angiography has low specificity for the diagnosis of glioblastoma multiforme (GBM). Although images may show vascular displacement on the basis of the mass effect of the tumor, virtually any other space-occupying lesion may have similar findings. In addition, the hypervascularity of GBM may mimic vascular malformations.

False Positives/Negatives

Any space-occupying lesion or vascular malformation with hypervascularity may cause a false-positive finding. Small tumors or those with a high infiltrative component and little or no vascular displacement may cause a false-negative finding.

INTERVENTION

Section 10 of 12  

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• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

The therapeutic approach to glioblastoma multiforme (GBM) consists of a combination of surgical resection, radiation therapy, and chemotherapy.^{27, 28, 29, 30}

Surgical resection is the mainstay of treatment. Complete resection is the surgeon's goal, but this is usually impossible because of several factors. For instance, the anatomic structures involved may prevent total resection. In addition, tumors usually extend beyond the visible margins on images.

Radiation therapy usually follows surgery. Radiation therapy may include whole-brain therapy, gamma-knife therapy, particle therapy, and/or brachytherapy. This treatment may also include the use of radioactive seed implants placed on the resection bed at the time of surgery. Gliomatosis cerebri is more radiosensitive than GBM.

Many chemotherapeutic regimens exist.

Experimental regimens that have, so far, met with limited success include genetic studies of TP53 with the administration of p53 protein or gene to tumor, injections of antigenic particles into the tumor to stimulate immune response against it, and interleukin therapy.²⁷

Medical/Legal Pitfalls

• The main pitfalls are related to diagnosis of the tumor. A small low-grade glioma that is missed with a screening study may eventually progress to glioblastoma multiforme.
• In addition, because of the highly variable appearance of the tumor, it may sometimes mimic other conditions, such as an infarct, an abscess, or even a tumefactive plaque in multiple sclerosis, and thereby delay diagnosis.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  T1-weighted axial gadolinium-enhanced MRI demonstrates an enhancing tumor of the right frontal lobe. Image courtesy of George Jallo, MD.
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Media file 2:  T2-weighted image demonstrates the same lesion as in Image 5 with notable edema and midline shift. This finding is consistent with a high grade or malignant tumor. Image courtesy of George Jallo, MD.
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Media file 3:  Axial T1-weighted gadolinium-enhanced MRI demonstrates the malignant glioma in the left thalamus, with mass effect and hydrocephalus. Image courtesy of George Jallo, MD.
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Media file 4:  Axial T2-weighted image confirms the location of the same tumor as shown in Image 7. Image courtesy of George Jallo, MD.
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Media type:  Image

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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2. American Cancer Society. What Are Brain and Spinal Cord Tumors in Children?. American Cancer Society: Cancer Reference Information. Available at http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_are_childrens_brain_and_spinal_cord_tumors_4.asp?sitearea=. Accessed May 22, 2008.
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13. Ducray F, Idbaih A, de Reynies A, Bieche I, Thillet J, Mokhtari K, et al. Anaplastic oligodendrogliomas with 1p19q codeletion have a proneural gene expression profile. Mol Cancer. May 20 2008;7(1):41. [Medline].
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25. Andersen PB, Blinkenberg M, Lassen U, Kosteljanetz M, Wagner A, Poulsen HS, et al. A prospective PET study of patients with glioblastoma multiforme. Acta Neurol Scand. Jun 2006;113(6):412-8. [Medline].
26. Cha S, Lupo JM, Chen MH, Lamborn KR, McDermott MW, Berger MS, et al. Differentiation of glioblastoma multiforme and single brain metastasis by peak height and percentage of signal intensity recovery derived from dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging. AJNR Am J Neuroradiol. Jun-Jul 2007;28(6):1078-84. [Medline].
27. Wong ET, Brem S. Antiangiogenesis treatment for glioblastoma multiforme: challenges and opportunities. J Natl Compr Canc Netw. May 2008;6(5):515-22. [Medline].
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Article Last Updated: Jul 2, 2008