CASE REPORTJ Neurosurg Pediatr 21:428–433, 2018

Choroid plexus adenomas are a rare, benign sub-set of choroid plexus tumors that the 2016 World Health Organization Histological Classification

of Tumours of the Central Nervous System does not sepa-rately categorize.14 Although they occur across a broad age range, these tumors have been reported in only 4 cases in the pediatric age group.4,17 As these tumors are mainly intraventricular, children usually present with hy-drocephalus. Radiographically, the tumors are difficult to differentiate from the more common choroid plexus tumors; therefore, recognition of the histological pattern becomes paramount for diagnosis. Here, we present a pe-diatric case of a choroid plexus adenoma whose unusual location, imaging characteristics, and histopathological features expand the phenotype of this rare tumor.

Case ReportHistory and Examination

An 8-year-old boy with an 18-month history of head-aches presented to the emergency department with an intense headache followed by emesis and lethargy. On presentation, the patient’s neurological examination find-

ings were normal, except for intermittent staring spells. A head CT scan was obtained and revealed a calcified mass in the deep left cerebral hemisphere, abutting the left lat-eral ventricle with solid and cystic components, without ventricular enlargement (Fig. 1 left). Subsequent MRI of the brain with and without contrast revealed a large, 4.0 × 3.5 × 3.3–cm, solid and multiloculated cystic mass located in the left parietal lobe adjacent to the left lateral ventricle and extending posteriorly into the body of the corpus cal-losum (Fig. 1 right). Perfusion MRI indicated increased cerebral perfusion within the solid enhancing mass. MRI findings were suggestive of a low-grade neoplasm, such as pleomorphic xanthoastrocytoma (PXA) or pilocytic astro-cytoma.

OperationThe patient underwent a left parietal craniotomy via

a superior parietal lobule approach to his deep left hemi-spheric tumor. Intraoperatively, the tumor was noted to be largely intraparenchymal and heavily calcified with mul-tiple cystic areas. There was no significant vascularity. On its most medial aspect, the tumor involved the wall of the atrium as well as the choroid plexus. Intraoperative path-

ABBREVIATIONS EMA = epithelial membrane antigen; GFAP = glial fibrillary acidic protein; PXA = pleomorphic xanthoastrocytoma.SUBMITTED June 5, 2017. ACCEPTED October 17, 2017.INCLUDE WHEN CITING Published online February 2, 2018; DOI: 10.3171/2017.10.PEDS17290.

Choroid plexus adenoma in a child: expanding the clinical and pathological spectrumNicole Prendergast, BS,1 Jeffrey D. Goldstein, MD,2 and Alexandra D. Beier, DO3

1Frank H. Netter MD School of Medicine, Quinnipiac University, North Haven, Connecticut; 2Department of Pathology and Laboratory Medicine, Mattel Children’s Hospital and Ronald Reagan UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California; and 3Division of Pediatric Neurosurgery, University of Florida Health, Jacksonville, Florida

Primary choroid plexus tumors encompass a variety of tumors, with choroid plexus papilloma and carcinoma being the most common. Also in the differential diagnosis is the rare benign choroid plexus adenoma. As these tumors are infre-quently described, the histological profile continues to evolve. The authors present a case with unusual characteristics that will broaden the pathological spectrum for choroid plexus adenomas.https://thejns.org/doi/abs/10.3171/2017.10.PEDS17290KEY WORDS pediatric; brain tumor; choroid plexus; oncology

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ological evaluation was interpreted as a low-grade glial neoplasm with Rosenthal fibers, calcifications, and cyto-logical features suggestive of PXA. Complete resection was achieved and confirmed on postoperative imaging (Fig. 2). The patient tolerated weaning of his external ven-tricular drain and was discharged on postoperative day 5 without complications. At his 1-year postoperative evalu-ation, the patient was neurologically well with no signs of recurrence on routine imaging.

Histopathological ExaminationEvaluation of the tumor revealed an epithelial neo-

plasm with large cells arranged in solid cords, nests, ir-regular tubules, and pseudoalveolar structures (Fig. 3A). The cells had eosinophilic cytoplasm and prominent nu-clear size variation, hyperchromasia, and multinucleation. Mitoses were not identified (Fig. 3B). The tumor invaded adjacent brain, invoking prominent piloid gliosis contain-ing numerous Rosenthal fibers (Fig. 3C). A similar reac-tion was present between the tumor cords and nests, and a biopsy of the cyst wall showed only piloid gliosis with occasional Rosenthal fibers, but no neoplastic epithelium. No xanthomatous change was seen within the tumor cells, and numerous microcalcifications exhibited a laminated psammomatous appearance (Fig. 3D).

Immunohistochemical staining with a panel of epithe-lial, glial, neural, and neuroendocrine markers was positive for broad-spectrum cytokeratins AE1/AE3 and CAM 5.2, and scattered positivity of cytokeratins 7 and 20, S100 pro-tein, syanptophysin, and nonphosphorylated neurofilament protein. The tumor was negative for glial fibrillary acidic protein (GFAP), epithelial membrane antigen (EMA), chromogranin, and NeuN. INI1 (SMARCB1) expression was retained, excluding a cribriform neuroepithelial tumor. The Ki-67 proliferative index was low (1%–2%).

Although the aberrant reactivity for neurofilament re-mains unexplained, choroid plexus tumors may express S100 protein and synaptophysin, which are usually not expressed by other epithelial tumors. These immunohis-tochemical reactions, together with the overt glandular epithelial architecture, favored the diagnosis of a choroid plexus adenoma. New novel markers of choroid plexus

papilloma, Kir7.1, and stannicalcin-1 were not available to apply to this case. The nuclear atypia was regarded as a degenerative change in a very indolent and slow-growing neoplasm. Although the extension into adjacent cerebral tissue was recognized, the tumor remained classified as WHO grade I based on its low proliferative potential.

DiscussionChoroid plexus tumors are rare, intraventricular, papil-

lary neoplasms of neuroectodermal origin that constitute less than 1% of brain tumors in adults and about 2%–5% in the pediatric population, most commonly in children younger than 2 years.5,13–15 Choroid plexus papillomas are most frequent and are associated with long-term survival when compared with choroid plexus carcinomas, which are aggressive lesions with a poorer prognosis.5 Choroid plexus adenomas are even rarer, benign tumors of the cho-roid plexus. Only 12 previous cases have been reported, with only 4 cases in the pediatric population (Table 1).1–4,

6, 8,10,12,17,18,21–24 These tumors are not mentioned in prior or the most recent WHO classification, and some may regard them as an unusual growth pattern of choroid plexus ad-enoma.14

Recent studies have identified chromosomal copy num-ber, methylation, and gene expression patterns in choroid plexus tumors that may be helpful in defining oncogenesis, predicting outcome, and potentially identifying agents for targeted therapy. These include greater numbers of chro-mosomal losses, increased acquired uniparental disomy, and somatic TP53 mutations in choroid plexus carcino-mas, as opposed to papillomas.16 Methylation of genes

FIG. 1. Left: Axial CT scan of the head without contrast, revealing a left cerebral calcified mass. Right: Axial MR image of the brain with con-trast, depicting a multicystic enhancing mass.

FIG. 2. Axial MR image of the brain with contrast, detailing resection of the mass.

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in the tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) pathway, activation of Notch3 and plate-let-derived growth factor receptors, and overexpression of the transcription factor TWIST1 (an inhibitor of p53) are proposed mechanisms contributing to choroid plexus neo-plasia.19 No cytogenetic or molecular studies could be per-formed in our case; thus, the degree to which this case of choroid plexus adenoma may resemble more conventional choroid plexus tumors remains unknown.

The majority of choroid plexus tumors present with signs of increased intracranial pressure and hydrocepha-lus.5 In the 4 previous reported pediatric cases of choroid plexus adenomas, 2 patients presented with hydrocephalus and raised intracranial pressure, while the other patients presented with myoclonic seizures and dysphasia.4,10, 21,24 Hydrocephalus is thought to occur due to obstruction of the CSF pathway, overproduction of CSF by the tumor, impaired CSF absorption, or a combination of these fac-tors.7,13 Varga et al. noted that it is possible that hypersecre-

tion of CSF, although prevalent in papillomas, may not be inherent to choroid plexus adenomas.24 Although signifi-cant hydrocephalus is common, not all choroid plexus tu-mors overproduce CSF, and the lack of hydrocephalus and ventricular dilation on imaging should not exclude these tumors from the differential diagnosis.

In children, both choroid plexus papillomas and car-cinomas are most often located in ventricles.5 In a study involving 107 papillomas and 95 carcinomas, only 11% were extraventricular.9 Of the previously described pedi-atric cases of choroid plexus adenomas, all of the tumors originated in the ventricles; 3 occurred in the lateral ven-tricle and the fourth in the third ventricle.5,10,21,24 In the present case, the tumor was identified intraoperatively as extending to the ventricular surface. It was primarily with-in and infiltrative into the cerebrum, which has not been described in the pediatric population, thus confounding the current case’s differential diagnosis based on imaging findings.

FIG. 3. A: Choroid plexus adenoma with irregular tubules and pseudoalveolar spaces. Small intraluminal calcifications are also visible (arrows). Original magnification ×10. B: Prominent nuclear size variation, hyperchromasia and multinucleation (arrows), but mitoses were not identified. Original magnification ×40. C: Piloid gliosis with abundant Rosenthal fibers (left side and arrows) where tumor cells invaded into adjacent brain. Original magnification ×20. D: Area of confluent psammomatous microcalcifica-tions (arrows). Original magnification ×20. Figure is available in color online only.

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N. Prendergast et al.TA

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Histologically, choroid plexus adenomas are character-ized by the lack of papillary, fibrovascular fronds present in choroid plexus papillomas. They are described as hav-ing well-differentiated neoplastic tubular glands and ir-regularly shaped acini.17 The basement membrane in pre-viously reported cases was continuous and covered by cu-boidal cells. These tumors lacked mitotic figures, nuclear atypia, or necrosis seen in choroid plexus carcinomas.4,17 In evaluating the immunohistochemistry in the previous cases, including both adult and pediatric tumors, they have shown expression of S100 protein, vimentin, transthyre-tin, and cytokeratin. Aside from the pediatric case pre-sented by Aquilina et al., most cases have been negative for GFAP. When used, adenomas have previously been negative for CAM 5.2, EMA, and cytokeratins 7 and 20, which highlights the variability as the current case reveals positivity of CAM 5.2 and cytokeratins 7 and 20.4,17

Morphological variations of choroid plexus papillomas and carcinomas exist and include oncocytic transforma-tion, dystrophic calcification, melanosis, and osseous metaplasia. Calcifications have previously been variably seen in choroid plexus adenomas.17 We found significant calcification and pronounced piloid astrocytosis with Rosenthal fibers, which has not been described previously. This feature and the calcification are indicators of an in-dolent, long-standing tumor. Multinucleation and degen-erative cytological atypia are also previously undescribed features in choroid plexus adenoma, lending to the evolv-ing pathological description of this type of tumor.

In addition to the tumors in the differential diagnosis based on the location near the ventricle and choroid plex-us, other tumors that radiographically can be considered are PXA and the recently described cribriform neuroepi-thelial tumor. PXAs are generally cystic with a contrast-enhancing mass similar to the MRI findings in this case, and the cytological atypia and gliosis in the current case also resembled PXA. However, one main differentiating feature is that PXAs stain positive for GFAP.20 In addition, cribriform neuroepithelial tumors that can have similar radiographic appearances are differentiated by their EMA reactivity and exhibit loss of SMARCB1 (INI1).11 It is ben-eficial to know the differential diagnosis of choroid plexus tumors preoperatively as it can guide surgical approach and management. In terms of treatment options, on initial imaging, it can be difficult to differentiate benign tumors from high-grade lesions. Therefore, surgery has been the mainstay treatment for choroid plexus adenomas, with some cases requiring multiple stages.21 Although gross-total resection is preferred, as these are benign lesions, subtotal resection and/or biopsy has been reported with good outcomes.2,4

ConclusionsWe have highlighted a pediatric case of choroid plexus

adenoma to expand the current differential diagnosis and morphological spectrum for these types of tumors. As these tumors can initially be thought to be higher-grade lesions, thus prompting resection, careful pathological analysis is required as aggressive surgery may not be re-quired in surgically challenging tumors.TA

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AcknowledgmentsWe appreciate the consultation and assistance of Dr. Peter

Burger, Johns Hopkins Medicine, in the evaluation of this patient’s specimen. We also thank Kelsey Hayward for her assistance in manuscript preparation.

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3. Andreini L, Doglioni C, Giangaspero F: Tubular adenoma of choroid plexus: a case report. Clin Neuropathol 10:137–140, 1991

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DisclosuresThe authors report no conflict of interest concerning the materi-als or methods used in this study or the findings specified in this paper.

Author ContributionsConception and design: Beier. Acquisition of data: Beier, Gold-stein. Analysis and interpretation of data: Goldstein. Drafting the article: Prendergast, Goldstein. Critically revising the article: all authors. Reviewed submitted version of manuscript: Beier. Approved the final version of the manuscript on behalf of all authors: Beier. Study supervision: Beier.

CorrespondenceAlexandra D. Beier: University of Florida Health, Jacksonville, FL. alexandra.beier@jax.ufl.edu.

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