Glioblastoma (GBM) is a WHO grade 4 glial tumor and the most common primary malignant brain tumor in adults. It is typically supratentorial in location and can spread to the contralateral hemisphere through the corpus callosum (butterfly glioma). Histologically, it contains necrosis and microvascular proliferation. IDH-wildtype GBM is the most aggressive subtype with a median survival of 14-16 months. Combined temozolomide and radiotherapy is the standard treatment approach.
Age Range
50-80
Peak Age
65
Gender
Male predominant
Prevalence
Common
Glioblastoma is an extremely aggressive tumor arising from astrocytic glial cells. Due to rapid cell proliferation, the tumor outgrows its blood supply, resulting in characteristic central necrosis surrounded by palisading tumor cells. Intense neoangiogenesis produces new vessels with abnormal permeability, which manifests on MRI as ring-like contrast enhancement and surrounding vasogenic edema. Tumor cells demonstrate infiltrative spread along white matter tracts; this feature appears on T2/FLAIR sequences as signal hyperintensity extending far beyond the enhancing component. High cellularity and mitotic activity manifest as restricted diffusion on DWI and elevated choline with reduced NAA on MR spectroscopy. Elevated rCBV values on perfusion MRI serve as quantitative markers of neoangiogenesis.
Thick (>3-4mm) and irregular ring-like enhancement with central necrotic area on T1 post-contrast sequences is the most characteristic and diagnostic imaging finding of GBM. Wall thickness is asymmetric — the wall adjacent to cortex is usually thicker, while the wall facing deep white matter is thinner. This pattern corresponds to gadolinium leakage through disrupted blood-brain barrier of abnormal vessels formed by neoangiogenesis and coagulative necrosis in the tumor center.
On non-contrast CT, a heterogeneous mass lesion is observed. Central hypodensity represents necrosis, while peripheral isodense-to-mildly hyperdense areas correspond to viable tumor tissue. Foci of acute hemorrhage may be seen as hyperdense areas. Marked peritumoral edema causes surrounding parenchymal hypodensity and mass effect. Calcification is rare, and its presence should raise consideration of alternative diagnoses such as oligodendroglioma.
Report Sentence
A heterogeneous mass lesion measuring approximately _x_x_ cm is identified in the right/left frontoparietal region, containing a central hypodense necrotic component and a peripheral isodense solid component. Marked peritumoral edema and mass effect are present.
Contrast-enhanced CT demonstrates thick, irregular ring-like enhancement. The wall thickness is asymmetric; the medial wall is usually thinner than the lateral wall (due to infiltration toward deep white matter). The central necrotic area does not enhance. Marked vasogenic edema and mass effect are present in the surrounding parenchyma. Multifocal enhancement is seen in 20-30% of cases, suggesting multicentric disease.
Report Sentence
On contrast-enhanced series, the lesion demonstrates thick, irregular ring-like enhancement peripherally, with the central necrotic component showing no enhancement.
On T1-weighted sequences, a heterogeneous, predominantly hypointense mass lesion is observed. The central necrotic area is markedly hypointense. Solid components of the tumor appear iso-to-hypointense relative to gray matter. Intralesional hemorrhagic foci may be seen as T1 hyperintense areas (due to methemoglobin). On T1 post-contrast sequences, thick and irregular ring-like enhancement is the most characteristic imaging finding of GBM.
Report Sentence
On T1-weighted sequences, a heterogeneous hypointense mass is observed, demonstrating thick, irregular ring-like enhancement on post-contrast T1 sequences. The central necrotic component shows no enhancement.
On T2-weighted sequences, a heterogeneous hyperintense mass lesion is observed. The central necrotic area is markedly hyperintense (free fluid). Solid tumor components appear iso-to-hyperintense relative to cortex. Extensive T2 hyperintense vasogenic edema is present in the surrounding parenchyma, typically exceeding the mass size. Edema shows finger-like extension along white matter. A T2 hypointense rim ('dark rim') may be seen around the necrotic area in some cases, related to hemosiderin deposition. Marked mass effect with ventricular compression and midline shift may be observed.
Report Sentence
On T2-weighted sequences, a heterogeneous hyperintense mass is observed with markedly hyperintense central necrotic component. Extensive vasogenic edema and mass effect are present in the surrounding parenchyma.
On FLAIR sequences, extensive hyperintense signal abnormality is observed around the mass. While a significant portion of this signal change represents vasogenic edema, the extension of FLAIR abnormality beyond the enhancing component in GBM represents infiltrative tumor spread — this concept is termed 'non-enhancing tumor.' FLAIR is superior to T2 for detecting periventricular and cortical lesions as it suppresses CSF signal. FLAIR abnormality beyond enhancement is critical for surgical planning and radiotherapy target volume delineation. In the butterfly glioma pattern, FLAIR best demonstrates bilateral infiltration along the corpus callosum.
Report Sentence
On FLAIR sequences, extensive hyperintense signal abnormality extending beyond the enhancing component is observed, consistent with infiltrative tumor spread.
On diffusion-weighted imaging (DWI), restricted diffusion is observed in the solid tumor component — hyperintense on DWI and hypointense on ADC maps. The necrotic central area shows facilitated diffusion (high ADC values). DWI restriction is proportional to cellularity and correlates with tumor grade. ADC values are typically 700-1000 x10⁻⁶ mm²/s in the solid component. Minimum ADC value is inversely proportional to tumor grade and prognosis — lower ADC indicates more aggressive tumor. DWI is critical in differentiating from abscess: abscess cavity shows restricted diffusion, while GBM's necrotic center shows facilitated diffusion.
Report Sentence
Restricted diffusion is observed in the solid tumor component on DWI (ADC: ~___ x10⁻⁶ mm²/s), with facilitated diffusion in the central necrotic area.
On dynamic susceptibility contrast (DSC) perfusion MRI, markedly elevated relative cerebral blood volume (rCBV) is observed in the enhancing solid tumor component. rCBV values are typically >1.75 (relative to contralateral normal white matter), serving as a quantitative marker of neoangiogenesis. Maximum rCBV values are usually detected in the thickest portion of the ring enhancement. rCBV is low in the necrotic center. Elevated rCBV values in the peritumoral area suggest infiltrative tumor extending beyond enhancement — this finding is valuable in differentiating from metastasis (peritumoral edema of metastasis has normal or low rCBV). rCBV is the most reliable perfusion parameter for differentiating low-grade (grade 2) from high-grade (grade 3-4) gliomas.
Report Sentence
Perfusion MRI demonstrates markedly elevated rCBV values in the enhancing solid tumor component (rCBV: ___), consistent with high-grade glial tumor.
MR spectroscopy (MRS) demonstrates characteristic metabolite patterns for GBM. The choline (Cho) peak is markedly elevated — reflecting high membrane turnover and cell proliferation. N-acetyl aspartate (NAA) is markedly reduced — indicating neuronal damage and destruction. Cho/NAA ratio >2.0 is a strong finding favoring high-grade glioma. Cho/creatine ratio >2.5 typically indicates grade 4 tumor. Lipid and lactate peaks represent necrosis and anaerobic metabolism — GBM typically shows a prominent lipid-lactate complex. Myoinositol (mI) is elevated in low-grade gliomas but variable in GBM. Elevated Cho/NAA ratio in the peritumoral area supports infiltrative tumor beyond enhancement.
Report Sentence
MR spectroscopy of the solid tumor component demonstrates markedly elevated choline peak, reduced NAA, and a prominent lipid-lactate complex, consistent with high-grade glial neoplasm.
On susceptibility weighted imaging (SWI), multiple punctate and linear susceptibility foci are observed within the tumor. These foci represent microhemorrhage (hemosiderin deposition), neovascular structures, and rarely calcification. The degree of intratumoral susceptibility signal (ITSS) is directly proportional to tumor grade and aggressiveness. SWI is 3-6 times more sensitive than conventional T2* gradient echo sequences for hemorrhage detection. GBM typically shows prominent ITSS, while low-grade gliomas show minimal or no ITSS. Dilated tumor vascular structures may be seen as hypointense tubular structures on SWI.
Report Sentence
On SWI sequences, multiple punctate and linear susceptibility foci are observed within the tumor, consistent with intratumoral hemorrhage and neovascularity.
Criteria
IDH1/2 mutation negative, standard GBM definition per WHO 2021 classification. In the presence of TERT promoter mutation, EGFR amplification, or +7/-10 chromosome changes, even histologically grade 2-3 diffuse astrocytic tumors are classified as GBM (grade 4).
Distinct Features
Usually >55 years, de novo development (without low-grade precursor), typical ring enhancement and necrosis, poor prognosis (median survival 14-16 months). Markedly elevated rCBV on perfusion MRI. Prominent lipid-lactate peak on MR spectroscopy.
Criteria
GBM subtype demonstrating spread to both hemispheres through the corpus callosum. Butterfly-shaped appearance on axial sections is characteristic. Usually begins with involvement of the genu or splenium of corpus callosum.
Distinct Features
Bilateral hemisphere involvement, corpus callosum infiltration, most prominent bilateral white matter signal increase on FLAIR. Complete surgical resection is usually not achievable. Perfusion and DWI are critical for differentiation from lymphoma.
Criteria
Rare histological variant of GBM containing prominent nuclear pleomorphism and multinucleated giant cells. Constitutes 1-5% of IDH-wildtype GBM. Tends to occur in a younger age group.
Distinct Features
Usually well-circumscribed, peripheral location, in temporal or parietal lobe. Better prognosis compared to conventional GBM. Calcification may be seen more frequently on CT. Better-circumscribed appearance on imaging may be confused with metastasis or other circumscribed tumors.
Criteria
Biphasic variant of GBM containing glial (GFAP+) and sarcomatous (mesenchymal) components. Constitutes 2-8% of all GBMs. WHO grade 4 tumor.
Distinct Features
Usually in temporal lobe, may show dural attachment (can be confused with meningioma), may have extra-axial component. Dural tail-like enhancement can create difficulty in differentiation from meningioma. Bone invasion and extracranial metastasis are more common than conventional GBM.
Distinguishing Feature
Metastasis: multiple lesions at gray-white matter junction, vasogenic edema disproportionate to lesion size, normal rCBV in peritumoral area (non-infiltrative). GBM: usually single large lesion, elevated rCBV in peritumoral area (infiltrative spread), corpus callosum involvement, non-enhancing tumor component in FLAIR abnormality.
Distinguishing Feature
Abscess: thin and smooth ring enhancement, restricted diffusion within cavity (DWI bright, ADC low), low rCBV, amino acid/acetate/succinate peaks on MRS. GBM: thick and irregular ring enhancement, facilitated diffusion in necrotic center (ADC high), elevated rCBV, elevated choline and lipid-lactate peak on MRS.
Distinguishing Feature
Primary CNS lymphoma: homogeneous enhancement (necrosis rare), markedly restricted diffusion (very low ADC), low rCBV (avascular nature of lymphoma), periventricular distribution, shrinkage with steroids. GBM: ring enhancement and necrosis, elevated rCBV, no expected steroid response.
Distinguishing Feature
Low-grade astrocytoma: no or minimal enhancement, low rCBV (<1.75), elevated myoinositol on MRS, normal ADC values, slow growth. GBM: marked ring enhancement, elevated rCBV (>1.75), lipid-lactate peak on MRS, low ADC, rapid growth.
Distinguishing Feature
Toxoplasmosis: in immunosuppressed patients (HIV/AIDS), multiple ring-enhancing lesions in basal ganglia, 'eccentric target sign,' low rCBV, response to anti-toxoplasma treatment. GBM: in immunocompetent patients, usually single large lesion, elevated rCBV, no expected treatment response.
Urgency
emergencyManagement
Maximal güvenli cerrahi rezeksiyon + adjuvan kemoradyoterapi (Stupp protokolü: temozolomid + 60 Gy RT) + 6-12 siklus adjuvan temozolomid. MGMT metilasyonu temozolomid yanıtını öngörür. Tümör tedavi alanları (TTFields) ek tedavi seçeneğidir.Biopsy
NeededFollow-up
Cerrahi sonrası 24-72 saat içinde kontrastlı MRG (rezidü tümör değerlendirmesi). Kemoradyoterapi sırasında ve sonrasında her 2-3 ayda kontrastlı MRG. Psödoprogresyon (tedaviye bağlı kontrast tutulumu artışı) ilk 3-6 ayda sık görülür — RANO kriterlerine göre değerlendirilmelidir.Glioblastoma is the most aggressive primary brain tumor and requires urgent neurosurgical consultation. Rapid neurological deterioration may develop due to mass effect and edema, necessitating emergency decompressive surgery. Standard treatment consists of maximal safe resection followed by the Stupp protocol (concurrent temozolomide + radiotherapy + adjuvant temozolomide). MGMT promoter methylation is the strongest predictor of chemotherapy response. Advanced imaging techniques (perfusion, MRS, DWI) are critical for treatment response monitoring and pseudoprogression differential diagnosis.
GBM is the most aggressive primary brain tumor. Standard treatment includes maximal safe resection, radiotherapy, and temozolomide chemotherapy (Stupp protocol). MGMT promoter methylation is an important biomarker for treatment response and prognosis. IDH-wildtype GBM carries a worse prognosis.