Epidermoid Cyst of the Brainstem in Children

Abstract

Epidermoid cysts are rare, slow growing, space-occupying lesions of early adulthood. Among the various locations, involvement of the brainstem is quite exceptional. In children, these tumors are extremely uncommon; only 4 purely intrinsic brainstem epidermoids are reported in the literature. The pathogenesis of true intraaxial brainstem epidermoid is unclear and is usually not considered in the preoperative differential diagnosis of brainstem tumors. We report 2 additional cases of brainstem epidermoid cysts occurring in children, underlining their clinical characteristics, the difficulties faced in the diagnostic work-up, and the surgical treatment adopted. These tumors pose a surgical challenge and attempts at aggressive removal of the cyst wall are fraught with increased risks of morbidity and mortality. On the other hand, cases treated more conservatively show good or excellent results with minimal complications. Neurosurgical judgment at the time of surgery is warranted to ensure maximum resection while minimizing postoperative neurologic deficits.

Keywords

brainstem epidermoid cyst magnetic resonance imaging surgical treatment

Epidermoid cysts are rare intracranial space-occupying lesions that account for about 1% to 2% of all intracranial tumors; they are even rarer in the pediatric age group.^1–3 The most common location is the cerebellopontine angle and parasellar region^4–6; less frequently, they are located within the cerebral ventricles and brain parenchyma.^7,8 Posterior fossa epidermoids usually arise in the lateral subarachnoid cisterns,^4,9 and those involving the brainstem are rare.^2,10–14 These lesions can insinuate themselves into several intracranial compartments by filling the subarachnoid space, and they usually grow insidiously at a linear rate, causing slow onset of symptoms. True brainstem epidermoids without any exophytic component are even rarer but their pathogenesis is questionable.^{11,14,15–17} This location is difficult to explain. Some authors deny the possibility of an epidermoid cyst developing primarily inside the brainstem, and in fact argue that the apparent intra-axial location is the late result of a progressive invasion and splitting of the brainstem brought about by the growth of ectodermal remnants primarily developing around the basilar artery.¹³ Initial reports suggested a grim prognosis with high mortality from surgery and meningitis as a complication.

Brainstem epidermoids are extremely rare in children; so far, only scattered case reports have appeared in the literature dealing with this unusual location (Tables 1,2). Here we report our experience with 2 children harboring brainstem epidermoids; one of the epidermoids was intrinsic to the brainstem. The rather exceptional occurrence of such lesions prompted us to describe these cases in detail, to review the pertinent literature, and to analyze the specific problems faced as to diagnosis and management.

Table 1.

Literature Review of Pediatric Brainstem Epidermoid Cysts With Extraaxial Component

Authors	Age/sex	Location	Presentation	Signs	Management	Outcome
Bhatia et al,¹⁸ 1978	3.5 y/M	Extraaxial + PM	Ataxia, delayed milestones	Hemiparesis, papilledema, V, VI, UMN VII CN involvement	Shunt and aspiration	Died 2 weeks after surgery due to meningitis
Leal and Miles,¹² 1978	3.5 y/F	Extraaxial + Medulla	Recurrent episodes of meningitis, hemiparesis	Hemiparesis, papilledema, VI, LMN VII CN involvement	Aspiration and subtotal resection	Minimal improvement; developed posterior fossa abscess; died 2 mo later
Schwartz and Balentine,¹⁹ 1978	14 mo/F	Extraaxial + Pons	Recurrent episodes of meningitis, hemiparesis	Hemiparesis, VII CN involvement	Shunt	Died after progressive brainstem function deterioration; postmortem diagnosis
Radhakrishnan et al,²⁰ 1992	13 y/F	Extraaxial + PM	Headache, ataxia, difficulty in swallowing, diplopia	Papilledema, gaze palsy, diminished gag reflex, UMN VII CN involvement	Shunt, radiation	Died; postmortem diagnosis
Kuzeyli et al,²¹ 1996	2 y/M	Extraaxial + Pons	Headache, bad temper	Hemiparesis, UMN VII CN involvement	Subtotal resection	Asymptomatic at 5-mo follow-up
Caldarelli et al,¹⁰ 2001	18 mo/F	Extraaxial + PM	Behavioral alterations, gait unsteadiness	Neck stiffness	Gross total resection	Recurrence at 18 mo; reexploration, subtotal excision; stable residual at 3-y follow-up
Ziyal et al,²² 2005	5 y/F	Extraaxial + Medulla	Dysphagia, hoarseness	IX, X, XI, and XII CN palsies	Gross total resection	Lower cranial nerve palsy improved after surgery
Takahashi et al,²³ 2007	10 y/F	Extraaxial + PM	Difficulty in swallowing, vomiting	Bilateral VI CN paresis	ETV, aspiration, subtotal resection	Recurred thrice; definitive surgery fourth time, asymptomatic at 16-mo follow-up
Ahmed et al,²⁴ 2009	NA/F	Extraaxial + PM	NA	NA	Subtotal resection	NA
Present case 1	6 y/F	Extraaxial + Pons	Intermittent headache	None	Aspiration and subtotal resection	No postoperative deficits

Abbreviations: CN, cranial nerve; ETV, endoscopic third ventriculostomy; LMN, lower motor neuron; NA, not available; PM, pontomedullary; UMN, upper motor neuron.

Table 2.

Reported Cases of Pediatric Intrinsic Brainstem Epidermoid Cysts

Authors	Age/sex	Location	Presentation	Signs	Management	Outcome
Weaver and Coulon,¹⁴ 1979	1 y/M	Pons [intrinsic]	Diplopia, facial weakness	VI, LMN VII CN involvement	Aspiration and subtotal resection	Improved initially; symptom recurrence after 10 wk; bacterial meningitis
Fournier et al,¹¹ 1992	14 mo/M	PM [intrinsic]	Gait unsteadiness	Quadriparesis, ataxia, LMN VII CN involvement	Subtotal resection	Developed multiple recurrences; died 19 mo after surgery
Caldarelli et al,¹ 2004	2 y/F	PM [intrinsic]	Behavioral disturbance, cerebellar symptoms	NA	Subtotal resection	Recurrence managed by subtotal resection
Resinos et al,²⁵ 2006	17 mo/F	PM [intrinsic]	Hemiparesis, facial weakness, ataxia	VII CN palsy, horizontal gaze paresis	Gross total decompression	Asymptomatic at 2-y follow-up
Present case 2	2 y/M	PM [intrinsic]	Hemiparesis	Hemiparesis	Aspiration and gross total resection	Hemiparesis improved; no new deficits.

Abbreviations: CN, cranial nerve; ETV, endoscopic third ventriculostomy; LMN, lower motor neuron; NA, not available; PM, pontomedullary; UMN, upper motor neuron.

Case 1

A 6-year-old girl presented in our outpatient department 10 months back with complaints of mild, intermittent, holocranial headache without any other features of raised intracranial pressure. Her neurologic examination was normal. Initially she symptomatically improved with analgesics but due to recurring headache, she underwent magnetic resonance imaging (MRI) of the brain to rule out any intracranial pathology. MRI showed a well-defined extraaxial cystic lesion 26 × 21 mm anterior to the brainstem, hypointense on T1-weighted images and predominantly hyperintense on T2-weighted imaging (Figure 1A-C). A small area of hyperintensity was seen within the lesion on T1-weighted images. There was no evidence of enhancement after gadolinium injection. Part of the lesion showed restriction on diffusion weighted imaging. The possibility of a prepontine epidermoid cyst or neurenteric cyst was considered in the differential diagnosis. Because the patient was asymptomatic, arrangements were made for serial follow-up imaging sequences with the goal to perform surgery if any neurologic signs developed. Six months later the child was brought back with an increase in her headache frequency but without any neurologic deficits. Her examination was essentially normal. A repeat MRI was performed which showed that the lesion had almost doubled in size, causing compression and distortion of the brainstem (Figure 1D-H). A large part of the tumor was insinuating into the pons, almost reaching up to the fourth ventricle. The hyperintense signal that was noted within the lesion on T1-weighted images earlier had also increased in size (Figure 1D). Magnetic resonance spectroscopy demonstrated a lipid peak at the corresponding region (Figure 1I). In view of these new findings on MRI, possibilities considered were infected epidermoid, abscess, or colloid-like cyst with high protein content. On the basis of the size of the lesion and its continued growth characteristics, the decision to resect this lesion was made. With the patient in the lateral position, a right retrosigmoid craniotomy was performed. The wall of the tumor was pearly white in color and on aspiration, yellowish, thick pus-like fluid was drained. The entire cyst collapsed after removal of its content. The capsule was gradually separated from the surrounding neurovascular structures but a part of it adherent to the pons was left behind. At the end, the tumor bed was irrigated with hydrocortisone solution in Ringer lactate. After operation, the patient awakened without neurologic deficits and was discharged home on the fifth postoperative day. The final pathologic diagnosis was epidermoid tumor. The fluid on microscopy revealed plenty of polymorphonuclear cells, though bacteriologic culture was negative. Follow-up of the patient at 6 months did not reveal any recurrence on imaging, and the patient was relieved of her headache.

Case 2

A 2-year-old boy presented with progressive weakness of right upper and lower limbs of 2 months' duration. On presentation, cranial nerve examination was unremarkable. Motor examination revealed Medical Research Council Grade 3 spastic hemiparesis. Deep tendon reflexes were exaggerated in the right arm and leg. Babinski reflex was positive on the right side. Rest of the neurologic examination was normal. MRI revealed a well-defined, intrinsic tumor involving the pons and upper medulla. The lesion was hypointense on T1-weighted imaging with a hyperintense nodularity within it (Figure 2A). On T2-weighted images, the entire lesion was uniformly hyperintense (Figure 2B and C). There was restriction on diffusion-weighted imaging and small specks of enhancement were noted in the periphery of the tumor (Figure 2D-F). The location and the intraaxial nature of the mass lesion were unusual for an epidermoid, and extrapolating our experience with the previous case, the possibility of an infected epidermoid/abscess was considered, which could explain T1 hyperintensity due to high protein content and hyperintensity in diffusion imaging due to its viscous content. The child underwent exploration via a midline suboccipital craniectomy with neuromonitoring. The floor of the fourth ventricle appeared ballooned out but the surface was unremarkable. Shortly following an incision in the right suprafacial triangle, a milky-white fluid was drained from the lesion cavity. There was also some ordinary epidermoid cyst content in the periphery of the lesion cavity. This material was also removed. Ventrally, a thin pial lining was seen separating the lesion from the vertebrobasilar vessels. The cavity was irrigated repeatedly with hydrocortisone solution. In the postoperative period, the child developed meningitis that was managed with intravenous antibiotics. There were no new neurologic deficits. The child was discharged on the tenth postoperative day. Histopathologic examination of the material removed from the lesion revealed an epidermoid cyst. The fluid was bacteriologically sterile with polymorphonuclear cells on microscopy. At the 3-month follow-up, the hemiparesis had significantly improved and the child was ambulant normally.

Discussion

Epidermoid cysts or “pearly tumors” were first fully described by the French pathologist Cruveilhier in 1829.²⁶ Although congenital, they usually become symptomatic only in early adulthood as an effect of the inner accumulation of desquamated cell debris deriving from their capsule. An analysis of previous series of brainstem epidermoids revealed that almost half of the cases occurred in children and the duration of symptoms was short. This was in contradiction to epidermoids occurring in other intracranial locations.

Epidermoid cysts are thought to derive from ectodermal remnants that remain during closure of the neural tube between the third and fifth weeks of embryonic life.^5,27,28 Although this supposed etiology would account for a midline position within the craniospinal axis, most epidermoid tumors are found in a lateral position. Two main hypotheses have been propounded to justify these findings: (1) proliferation of multipotential embryonic cells or (2) lateral displacement of the included ectodermal cells driven by the developing otic and optic vesicles, which take place at a later embryologic stage.^4,11 The latter hypothesis seems to better account for the rare intraparenchymal epidermoid tumors. In such cases, in fact, the embryonic ectodermal remnants would reach their definitive site along the Virchow-Robin spaces, as they move together with the brain microvasculature.^9,29 In this regard, our first case seems to support the hypothesis of a primarily extraaxial origin of the cyst and the subsequent invasion and splitting of the brainstem.

Epidermoids grow usually within the basal cisterns displacing the neural and vascular structures. They contain waxy and pearly white material composed of desquamated keratin, cholesterol crystals, and cellular debris. The content is soft, cheesy, and putty-like. Creamy/milky fluid within an epidermoid cyst has rarely been reported.^22,30 Liquefaction of the cyst content may occur because of an intrauterine or childhood infection. This may result in rapid increase in size of these lesions with presentation in early childhood.

Clinical Symptomatology

The clinical symptoms depend on the location of the tumor and generally present in adulthood. The most common presentation of pediatric posterior fossa epidermoid tumors was cranial nerve involvement and cerebellar dysfunction.^9,31–33 Intermittent episodes of headache can be attributed to aseptic meningitis triggered by spillage of the highly irritative cyst contents into the subarachnoid space.^12,30 Clinical signs were absent in our first case, when considering the size and location of the cyst. This may be attributed to the plasticity of neural architecture as these lesions insinuate into the brainstem. Surprisingly, in the second case, the boy presented with only hemiparesis without any cranial nerve deficits.

Imaging

Epidermoid lesions possess specific imaging characteristics, and often resemble other cystic lesions of the brain. They present as a low-density mass on computed tomographic (CT) scan with no enhancement because of their low vascularity. Sometimes these tumors appear hyperdense on CT because of the presence of protein, lipid, calcium, and hemosiderin.³⁴ On MRI, their multilobulated appearance often helps determine the diagnosis. The signal intensity of an epidermoid cyst is variable and depends on the relative amount of lipid and to some extent on the amount of cholesterol and keratin within the tumor. On T1-weighted images, an epidermoid cyst usually shows signal intensity intermediate between brain and cerebrospinal fluid, and on T2-weighted images, it is usually hyperintense. T1 shortening is associated with cysts with high lipid/protein content. Nagashima et al³⁵ suggested that high protein concentration might be due to a proliferative and exudative defense reaction to recurrent minor leaks of the lipoid material through the capsule. On fluid-attenuated inversion recovery images, epidermoids appear hyperintense. Rarely, epidermoids can appear as a low-intensity lesion on fluid-attenuated inversion recovery sequences, making them appear similar to arachnoid cysts. This confusion, however, is resolved on close inspection of the diffusion-weighted images, which shows epidermoids to be distinctly bright compared with arachnoid cysts and other tumors.³⁶ Epidermoid cysts typically do not have peritumoral edema on T2-weighted images and do not show any contrast enhancement on gadolinium administration. The common differential diagnoses to be considered include arachnoid cysts, dermoids, lipomas, and cholesterol granulomas.³⁷

The MRI findings were complicated in our patients by the presence of a high-intensity area within the lesion on T1-weighted images. Epidermoid cyst and abscess are among those lesions that are usually hypointense on T1-weighted imaging but rarely can be hyperintense and mimic each other in different pulse sequences including diffusion-weighted imaging. High T1 signal intensity observed in the center of an abscess may correspond to a small amount of blood breakdown products in the proteinaceous purulent contents of the abscess. An infected neurenteric/neuroepithelial cyst may have the same imaging characteristics.³⁸ On magnetic resonance spectroscopy, abscesses have several peaks attributable to acetate, succinate, amino acids (alanine, valine, leucine, and isoleucine), and lactate. Epidermoid cysts show the peaks attributed to lactate and lipid but no amino acids, though this is not a hard-and-fast rule.²³ In both our cases, the presence of T1 hyperintensity within the lesion and restriction on diffusion-weighted imaging strongly suggested the preoperative diagnosis of epidermoid cyst. The pus-like, milky-white material aspirated during surgery showed plenty of polymorphonuclear cells on microscopy, though bacterial culture was negative, indicating conversion of the cyst into a sterile abscess. Thus, congenital/childhood infections could be a predisposing factor for liquefaction in pediatric epidermoids, and this may account for epidermoids involving the brainstem presenting in early childhood.

Treatment

The best treatment for epidermoid cyst is total removal. Although the cyst content can be removed easily,¹³ radical removal of the tumor capsule can be very difficult because of the firm adhesions to the surrounding neural and vascular structures. It is thought that the spillage of the contents of an epidermoid cyst into the subarachnoid space through small tears in the capsule can cause an intense inflammatory reaction between the capsule and underlying structures at times. This reaction can lead to dense adhesions between the capsule and cranial nerves and intracranial vessels.³⁹ This is especially true for brain stem epidermoid cysts where simple aspiration or subtotal excision of the tumor alone may be performed. Attempts to completely remove the capsule of lesions located inside the brainstem could be even more dangerous, as demonstrated by analysis of the experiences reported in the literature.^13,40,41 On the other hand, cases treated more conservatively showed good or excellent results with minor morbidity.^14,17,42 The incidence of postoperative aseptic meningitis resulting from spillage of the cyst content into the subarachnoid space during surgery ranges from 2% to 50%.^26,42–45

Obviously the major concern after a conservative resection is tumor recurrence. The recurrence rate is between 1% and 54%.^3,9,32,33,43 However, although tumor regrowth should be expected following partial/subtotal resections, the symptom-free interval before recurrence can be very long.

Conclusion

Brainstem epidermoids are extremely rare especially in the pediatric age group. The cause for liquefaction of the cyst contents is open to speculation. The rapid increase in size of the tumor and presence of pus cells within the cyst in our patients point toward a probable infective etiology. The absence of clinical signs in brainstem epidermoids can be attributed to neural plasticity that occurs as the tumor insinuates into the brainstem. The very existence of true intraaxial brainstem epidermoid is doubtful. The serial MRI done in our first case demonstrates the tumor growing into the brainstem providing support to the hypothesis that these lesions are in fact primarily extra-axial in origin. The subsequent invasion and splitting of the brainstem gives a false impression of an intrinsic lesion. Presence of hyperintensity within a pediatric brainstem cystic lesion on T1-weighted images coupled with restriction on diffusion-weighted imaging should alert one to a possibility of an infected epidermoid cyst. A lipid peak on magnetic resonance spectroscopy may be of additional value. Brainstem epidermoid should be managed by decompression of cyst contents and removal of nonadherent portions of the cyst capsule. Because epidermoid tumors are indolent, the risks of potential complications outweigh the benefits of total resection. Recurrence after partial removal, which occurs after a long time interval, does not justify total removal with unacceptable postoperative neurologic deficits.

Footnotes

CVG, AD, and SN prepared the original draft of this article. CVG and AD have made (1) substantial contributions to conception and design, acquisition of data, and analysis and interpretation of data; (2) drafted the article and revised it critically for content; and (3) approved the final version for publication. SN has been a mentor who has contributed equally to this work, taking part in the conception, drafting, and approval of the final version.

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

The authors received no financial support for the research, authorship, and/or publication of this article.

This article did not require ethical approval.

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