A 65-Year-Old Woman With a Left Occipital Lobe = Tumor

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TABLE OF CONTENTS

[REFERE= NCES]=20 [FI= GURES]

=A9=20 Copyright by College of American Pathologists 2006=20

Archives of Pathology and Laboratory = Medicine:=20 Vol. 130, No. 6, pp. e96=96e99.

A 65-Year-Old Woman With a Left Occipital Lobe Tumor

Sean J. Nagel, MD; Richard A. Prayson, MD; Robert J. Weil,=20 MD

From the Department of Neurosurgery (Dr Nagel), Department = of=20 Anatomic Pathology (Dr Prayson), and the Brain Tumor Institute, = Taussig=20 Cancer Center (Dr Weil), Cleveland Clinic Foundation, Cleveland,=20 Ohio

Accepted February 2, 2006

3D"" A 65-year-old, right-handed woman presented to an = outside=20 hospital complaining of left eye visual obscurations and headaches; mild = confusion was observed during physical examination. A noncontrast = computed=20 tomographic scan demonstrated left parietal-occipital edema. Clopidogrel = was=20 administered for presumed ischemic stroke. She returned 1 week later = with=20 persistent symptoms. A repeat computed tomographic scan demonstrated = progressive=20 intracerebral edema; a magnetic resonance image was obtained. Magnetic = resonance=20 imaging showed a 3.0 =D7 3.0-cm heterogeneously enhancing mass with a = necrotic=20 center and surrounding vasogenic edema (Figure,=20 A 3D"" ). The patient was administered dexamethasone and her = headaches=20 improved. A systemic workup detected only a benign, 1.0-cm adrenal mass. = Laboratory values were within normal limits.

3D"" The patient had a medical history significant for = non-Hodgkin=20 lymphoma (NHL), affecting the left inguinal lymph nodes, that had been = diagnosed=20 29 years earlier. She had been treated with chemotherapy and radiation = for 2=20 years. She had been routinely followed every 6 months since that time = and was=20 without known recurrence.

3D"" After completion of the course of dexamethasone, = the patient=20 underwent an image-guided, stereotactic, left parietal-occipital = craniotomy. A=20 tan-colored, friable tumor was identified beneath the cortical surface. = A=20 subtotal resection was performed. Pathologic examination of the resected = tumor=20 identified a diffuse, lymphocytic cell population with frequent mitosis = and an=20 angiocentric distribution (Figure,=20 B 3D"" , original magnification =D7200; Figure,=20 C 3D"" , original magnification =D7400). Immunophenotyping = revealed a=20 CD20-predominant B-cell population (Figure,=20 D 3D"" , original magnification =D7200), which also stained for = CD19; these=20 cells lacked CD10 and CD5.

3D"" What is your diagnosis?

Pathologic Diagnosis: Diffuse Large B-Cell, Primary Central = Nervous=20 System Lymphoma

Abstract

3D"" A 65-year-old woman with a medical history = significant for=20 remote non-Hodgkin lymphoma presented with confusion and visual = complaints.=20 Magnetic resonance imaging showed a parietal-occipital mass with = surrounding=20 vasogenic edema. The patient underwent a stereotactic, = parietal-occipital=20 craniotomy and biopsy of the lesion. A diagnosis of primary central = nervous=20 system lymphoma was made on the basis of histopathologic features and=20 immunophenotyping. A recent increase in the incidence of primary central = nervous=20 system lymphoma has been observed. These lymphomas are typically = angiocentric=20 with infiltration of intervening parenchyma by atypical lymphoic cells. = Patients=20 with previously diagnosed non-Hodgkin lymphoma are at increased risk for = a=20 second malignancy. Distinguishing primary central nervous system = lymphomas from=20 brain metastasis or other tumors is essential to therapy selection. = Advances in=20 the treatment of primary central nervous system lymphoma, specifically = with=20 high-dose methotrexate, has significantly improved long-term, = disease-free=20 survival.

3D"" Although histologically similar to other = non-Hodgkin types of=20 lymphomas, primary central nervous system lymphoma (PCNSL) is a = clinically=20 distinct disease entity, both in behavior and treatment. Primary central = nervous=20 system lymphoma is currently reported to account for up to 5% of primary = brain=20 neoplasms.¹=20 It is more common in patients who are immunosupressed; for example, its=20 incidence in patients with acquired immunodeficiency syndrome is as high = as=20 6%.²=20 However, immunocompromised patients, including those with the human=20 immunodeficiency virus as well as immunosuppressed transplant = recipients, only=20 partially account for a recent increased incidence of PCNSL.¹⁼⁹⁶³

3D"" In immunocompetent individuals, PCNSL has a peak = incidence in=20 the fifth to seventh decades of life.²=20 Patients with PCNSL often present with cognitive disturbance; however, a = new=20 focal deficit and/or seizure may be the first symptom of disease. The = disease=20 has suggestive, but not pathognomonic, neuroimaging features. In a = recent=20 retrospective review, 35% of patients with PCNSL had multifocal disease = at=20 presentation.⁴=20 Strong contrast enhancement and edema are characteristic of most = lesions.=20 Central necrosis, as seen on the magnetic resonance image of this = patient, is=20 more commonly a feature in patients with human immunodeficiency virus, = but is=20 infrequently observed in immunocompetent patients. In most instances,=20 stereotactic biopsy is sufficient to establish a diagnosis. If possible, = steroid=20 administration in clinically stable patients should be avoided prior to = biopsy=20 because steroids may induce tumor cell apoptosis and alter the = pathologic=20 picture.^2,⁵=20 Occasionally, a cerebrospinal fluid sample may be used in place of = tissue=20 biopsy. Distinguishing PCNSL from brain metastasis or other tumors is = essential=20 to the therapy that is selected. Given the presence of necrosis, a = feature seen=20 in only 6% of PCNSLs not associated with human immunodeficiency virus, = but seen=20 commonly in high-grade glial neoplasms such as glioblastoma, a = craniotomy was=20 performed in this patient.⁴=20 Once a diagnosis of lymphoma was established by frozen section, the = tumor was=20 only debulked.

3D"" Microscopically, PCNSLs are typically = angiocentric, with=20 infiltration of intervening parenchyma by atypical lymphoic cells. = Follicle=20 formations are not present. Lymphomatous foci may be present at distant = sites=20 within the brain that are not apparent on radiographic studies. There = are=20 usually frequent mitoses and an admixture of apoptotic cells or necrotic = foci.=20 Primary central nervous system lymphomas usually express B-cell markers, = including CD19, CD20, and CD79a. Only 2% of PCNSLs are of T-cell origin, = and=20 these often occur in the cerebellum.²=20 Although most primary lymphomas of the central nervous system (CNS) are = of the=20 diffuse large cell type, the pathologic subtype has not been shown to = confer a=20 survival advantage to date.⁶

3D"" Patients with previously diagnosed NHL are at = increased risk=20 for a second malignancy. This risk remains elevated even 2 decades after = diagnosis.⁷=20 Lymphoreticular neoplasms, such as leukemia and lymphoma, are the most = common=20 second cancer to occur in patients who have undergone radiation and/or=20 chemotherapy for prior malignancy, including NHL.⁸=20 The occurrence of a secondary PCNSL is less frequently observed in these = patients. Diagnosing PCNSL in patients with a history of NHL is = especially=20 challenging because the cancers may be remarkably similar. Only 5% of = patients=20 with an indolent variant of NHL will demonstrate CNS involvement. This = number=20 approaches 30% in more aggressive systemic lymphomas.⁹=20 Recurrences in the CNS are observed most often during the first 14 = months after=20 initial diagnosis.⁹

3D"" Disease recurrence in the CNS of patients with a = history of=20 extracerebral NHL cannot always reliably be excluded. However, previous=20 investigators have used the typical radiographic features, response to = steroids,=20 absence of systemic disease, and disease-free interval from the initial=20 malignancy to diagnose and initiate treatment.¹⁰=20 Additionally, leptomeningeal spread, rather than intraparenchymal = lesions, more=20 often portends metastatic involvement of extacerebral disease. = Regrettably in=20 this patient, the original tumor specimen from 29 years earlier had been = discarded by the outside hospital, so it was not possible to assess = tumor=20 clonality or compare immunophenotyping markers.

3D"" Patients with a diagnosis of PCNSL who are not = treated or are=20 treated only with steroids survive an average of 3 to 6 months.^2,⁵=20 Advances in the treatment of PCNSL during the past several decades have=20 significantly improved long-term, disease-free survival to 12 to 24 = months or=20 longer. Current treatment options include radiotherapy, corticosteroids, = chemotherapy, and stem-cell rescue and immunotherapy, either alone or in = combination. Age, Karnofsky performance status, and extent of disease = are=20 significant prognostic markers; survival is poorer for patients aged 60 = years=20 and older, those with a poor Karnofsky performance status, and in those = patients=20 with more extensive or multifocal CNS disease.^1,⁶

3D"" Corticosteroids have been shown to induce cellular = lysis in=20 mouse lymphoma cells. This experimental observation may explain tumor = regression=20 on radiographic images following steroid administration.⁵=20 Corticosteroids alone, however, have a negligible effect on patient = survival.=20 Whole-brain radiation therapy in conjunction with corticosteroids = improves the=20 median survival to 22 months; a dose of approximately 45 Gy is = recommended.⁶=20 Whole-brain radiation therapy in patients older than age 60 should be = limited=20 because of the neurotoxicitiy. Because patients with PCNSL typically = have=20 microscopic disease beyond the limits of neuroimaging-defined tumor, = focal=20 irradiation is not recommended.

3D"" Chemotherapy, and specifically methotrexate when = used in high=20 doses (>1 g/m²), is currently the mainstay in the = treatment of=20 PCNSL. Intrathecal methotrexate (injected into the lumbar subarachnoid = space or=20 via an indwelling Ommaya reservoir) has been used in patients with = cytologic=20 evidence of lymphoma cells in the cerebrospinal fluid. Blood-brain = barrier=20 disruption is another method used to increase the concentration of = methotrexate=20 in the CNS. The chemotherapy regimen selected should be completed prior = to=20 initiating whole-brain radiation therapy. Radiation disrupts the = blood-brain=20 barrier and potentiates the neurotoxic effects of chemotherapy on normal = brain.⁵=20 Blood-brain barrier disruption may obviate the need for whole-brain = radiation=20 therapy; studies are ongoing to test this hypothesis.¹¹

References Return= =20 to TOC

1. Hoang-Xuan K, = Camilleri-Broet=20 S, Soussain C. Recent advance in primary CNS lymphoma. Curr Opin = Oncol=20 2004;16:601=96606. [PubMed=20 Citation]

2. Schlegel U,=20 Schmidt-Wolf IGH, Deckert M. Primary CNS lymphoma: clinical = presentation,=20 pathological classification, molecular pathogenesis and treatment. J = Neurol=20 Sci 2000;181:1=9612. [PubMed=20 Citation]

3. Batara JF,=20 Grossman SA. Primary central nervous system lymphomas. Curr Opin = Neurol=20 2003;16:671=96675. [PubMed=20 Citation]

4. K=FCker W,=20 N=E4gele T, Korfel A. et al. Primary central nervous system lymphoma = (PCNSL): MRI=20 features at presentation in 100 patients. J Neurooncol = 2005;72:169=96177.=20 [PubMed=20 Citation]

5. DeAngelis LM,=20 Hormigo A. Treatment of primary central nervous system lymphoma. = Semin=20 Oncol 2004;31:684=96692. [PubMed=20 Citation]

6. DeAngelis LM,=20 Yahalom J. Lymphomas, section 4: Primary central nervous system = lymphoma. In:=20 DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and = Practice of=20 Oncology. 7th ed. Philadelphia, Pa: Lippincott Williams & = Wilkins;=20 2005:2012=962020.

7. Travis LB,=20 Curtis RE, Glimelius B. Second cancers among long-term survivors of non=20 Hodgkin's lymphoma. J Natl Cancer Inst 1993;85:1932=961937. [PubMed=20 Citation]

8. Reni = M,=20 Ferreri AJM, Zoldan MC, Villa E. Primary brain lymphomas in patients = with a=20 prior or concomitant malignancy. J Neurooncol 1997;32:135=96142. = [PubMed=20 Citation]

9. Lossos A,=20 Ashhab Y, Sverdin E. et al. Late-delayed cerebral involvement in = systemic=20 non-Hodgkin lymphoma: a second primary tumor or a tardy recurrence?.=20 Cancer 2004;101:1843=961849.

10. DeAngelis LM. Primary = central nervous=20 system lymphoma as a secondary malignancy. Cancer = 1991;67:1431=961435.=20

11. Blood-brain = barrier=20 disruption trial, Cleveland Clinic IRB no. 3669B. Available at: www.clevelandclinic.org/neuroscience/trials/brain/3669.htm. Accessed June 8, 2005.

Figures Return= =20 to TOC

Click on thumbnail for full-sized = image.

3D""=20

The authors have no relevant financial interest in the = products or=20 companies described in this article.

Corresponding author: Sean J. = Nagel, MD,=20 Department of Neurosurgery, S80, Cleveland Clinic Foundation, 9500 = Euclid Ave,=20 Cleveland, OH 44195 (E-mail: nagels@ccf.org)

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