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OtherCONTINUING EDUCATION

PET in Differentiation of Recurrent Brain Tumor from Radiation Injury*

Daniel D. Langleben and George M. Segall
Journal of Nuclear Medicine November 2000, 41 (11) 1861-1867;
Daniel D. Langleben
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George M. Segall
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  • FIGURE 1.
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    FIGURE 1.

    Sixty-y-old woman with stage IV ovarian cancer (diagnosed Sept. 1993) treated with surgery and chemotherapy until April 1994. (A) GdDTPA T1-weighted (Tr = 766, TE = 13) MRI scan (performed April 4, 1997) showing ring-enhancing lesions with central low signal in the right parietal cortex, the white matter of the right frontal lobe, and the right caudate head and anterior portion of the internal capsule. (B) PET scan (performed April 2, 1997) shows 2 right parietal cortical hypermetabolic lesions, hypometabolism in right frontoparietal area, and 2 areas of annular hypermetabolism with central hypometabolism: in the right frontal white matter and adjacent to the right caudate. In 1995, patient developed ataxia and right-sided hearing problems. MRI showed 2 right parietal metastases. Patient was treated with whole-brain radiation (30 Gy in 10 fractions) and dexamethasone and then with stereotactic radiosurgery (18 Gy to right parietal lesions). She developed seizures 8 mo later; MRI showed enlargement of 2 right parietal lesions. On April 4, 1997, she had stereotactic removal of the superficial lesions that were hypermetabolic on PET. Deeper lesions could not be removed because of location. Patient was lost to follow up after this procedure.

  • FIGURE 2.
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    FIGURE 2.

    MR and PET scans of 50-y-old man, with a history of grade 2 right frontal oligodendroglioma, who presented with headaches and memory loss. (A) GdDTPA T1-weighted (Tr = 700, TE = 16) MR scan of 50-y-old man, showing an area of low signal in the right parietal lobe with predominantly peripheral contrast enhancement, edema, and focal areas of hemorrhage, which indicated the possibility of tumor or DLRI. (B) PET scan of patient's brain, showing hypometabolic right frontoparietal area consistent with changes after surgery and radiation. No hypermetabolic foci to suggest recurrent tumor. Tumor was resected on September 8, 1993, and treated with radiation therapy to the frontal and parietal lobes (total dose between September 29 and November 9, 1993 = 56 Gy). Patient continued to have mild cognitive deficits and psychosis. In 1995, patient developed new neurologic deficits and dementia worsened. MR showed progression of edema and enhancement in the right parietal lobe, next to the resection site. PET scan in November 1995 was negative for abnormal hypermetabolic foci; a second craniotomy was performed December 1995, and right frontoparietal cystic lesion without evidence of malignancy on a frozen section was removed. Histologic examination showed mixed astrocytoma and oligodendroglioma without mitotic activity, and with areas of focal necrosis. Patient died in February 1996.

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    TABLE 1.

    WHO Classification of Primary Intracranial Tumors

    Classification
    NeuroepithelialCranial and spinal nervesMeningesLymphomas and hematopoietic tissueGerm cellCysts and tumor-like lesions
    Astrocytoma Oligodendroglioma Ependymoma Mixed choroid plexus Uncertain neuronal Pineal EmbryonalSchwannoma Neurofibroma MPNSTMeningioma (all variants) Anaplastic meningioma Benign mesenchymal Malignant mesenchymal Primary melanocytic UncertainMalignant lymphoma Plasmacytoma Granulocytic sarcoma OthersGerminoma Embryonal carcinoma Yolk sac Choriocarcinoma Teratoma Mixed germ cellRathke cleft Epidermoid Dermoid Colloid Enterogenous neuroglial Granular cell Hypothalamic Hamartoma Plasma cell Granuloma
    • MPNST, malignant peripheral nerve sheath tumor.

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    TABLE 2.

    Classification of Astrocytomas

    Kernohan (1940)Mayo/St. Anne (1981/1988)WHO grade (1979/1993)WHO designationHistopathology
    Grade 1ExcludedIPilocytic astrocytomaBipolar, piloid cells, Rosenthal fibers, eosinophilic granular bodies
    Grade 1Grades 1 and 2IILow-grade astrocytomaNeoplastic fibrillary or gemistocytic astrocytes; nuclear atypia
    Grade 2Grade 3IIIAnaplastic astrocytomaNeoplastic fibrillary or gemistocytic astrocytes; nuclear atypia mitotic activity
    Grade 3 Grade 4Grade 4IVGlioblastoma multiformeCellular anaplasia, nuclear atypia, mitoses, vascular proliferation, necrosis
    • Table modified from Kleihues (3) and Tatter (6).

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    TABLE 3.

    Clinical, Radiologic, and Pathologic Findings in Brain Radiation Injury

    Stage (time to onset)SymptomsMRI/CTPETPathology
    Acute (hours to weeks)Related to mass effect and ensuing increased ICP (headache, vomiting, altered consciousness)Edema; enhancing tumor massHypometabolismEdema; demyelinating plaques; gray–white junction fibrin exudate; hemorrhageic coagulation necrosis and vascular proliferation
    Early delayed (weeks to 4 mo)Mixed 1 and 3White matter cyst formationHypometabolismMixed 1 and 3
    Late delayed (4 mo to years)Focal neurologic deficits depending on the size and location of the lesionCortical atrophy Diffuse periventricular edema Expansile enhancing mass with focal hyperintensity on T2 and proton density imagesHypometabolismFibrinoid necrosis of the medium and small arteries with vascular proliferation; swollen gyri; hemorrhagic coagulation necrosis of the gray matter; white matter affected more than gray; axonal swelling, multifocal demyelination, hyalinization, and reactive gliosis
    ChronicStable focal neurologic deficits as well as global effects causing personality changes and dementiaVascular dystrophic calcification with cystic changes; cortical atrophy; telangioectasiaHypometabolismReactive gliosis; subcortical cyst formation; vasculitis, arteritis, enhanced atherosclerosis, and vascular dystrophic calcification with cystic changes
    • View popup
    TABLE 4.

    Accuracy of PET in Differentiation of Radiation Injury from Tumor Recurrence

    StudynPathologySensitivitySpecificityPPVNPV
    Patronas et al. (25)5Low-grade glioma100100
    Doyle et al. (26)9High-grade glioma100100
    Di Chiro et al. (17)95Glioma + metastases100100
    Valk et al. (24)38Glioma81887989
    Janus et al. (18)20Glioma83637771
    Davis et al. (12)35Glioma, lymphoma metastases83No data
    Kahn et al. (28)19Glioma (n = 17), other (n = 2)8140
    Kim et al. (27)33Glioma + metastases80949285
    Ricci et al. (21)31Glioma86568046
    • PPV, positive predictive values; NPV, negative predictive values.

    • View popup
    TABLE 5.

    Median Survival with Negative or Positive FDG PET

    StudynTumor typeMedian survival
    PET positivePET negative
    Patronas et al. (25)45Grade 3-4 glioma5 months19 months
    Mogard et al. (31)11Metastases0% in 54 weeks80% 1.7 years
    Ericson et al. (29)31Metastases12.3 months19.9 months
    Barker et al. (30)55Grade 3-4 glioma10 months20 months
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Journal of Nuclear Medicine
Vol. 41, Issue 11
November 1, 2000
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PET in Differentiation of Recurrent Brain Tumor from Radiation Injury*
Daniel D. Langleben, George M. Segall
Journal of Nuclear Medicine Nov 2000, 41 (11) 1861-1867;

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PET in Differentiation of Recurrent Brain Tumor from Radiation Injury*
Daniel D. Langleben, George M. Segall
Journal of Nuclear Medicine Nov 2000, 41 (11) 1861-1867;
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    • TREATMENT
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  • Multimodality Assessment of Brain Tumors and Tumor Recurrence
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  • Permeability Estimates in Histopathology-Proved Treatment-Induced Necrosis Using Perfusion CT: Can These Add to Other Perfusion Parameters in Differentiating from Recurrent/Progressive Tumors?
  • An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model
  • MR Spectroscopy in Radiation Injury
  • NCCN Task Force: Clinical Utility of PET in a Variety of Tumor Types
  • Clinical Applications of PET in Brain Tumors
  • Uptake of 18F-Fluorocholine, 18F-FET, and 18F-FDG in C6 Gliomas and Correlation with 131I-SIP(L19), a Marker of Angiogenesis
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