Squamous Cell Carcinoma Arising in an Epidermoid Cyst of Cavernous Sinus: A Rare Occurrence

Keywords

squamous cell carcinoma - cavernous sinus - epidermoid cyst

Introduction

An epidermoid cyst (EC) is slow-growing lesion of developmental origin, accounting for 0.2 to 1.8% of all the intracranial tumors. It arises from the aberrant inclusions of the ectodermal remnants that fail to regress between the third and fifth weeks of intrauterine life after completion of neural embryogenesis.[1] The most frequent locations of their occurrence are the cerebellopontine angle (CPA), parasellar region, middle cranial fossa, and prepontine cistern, and are extremely rare in the cavernous sinus.[2] They are benign but rarely can undergo malignant transformation to squamous cell carcinoma (SCC). This transformation has not yet been reported in the cavernous sinus. By far, intracranial SCC manifests as metastases from a primary, located outside the central nervous system or as a result of direct local spread from a head and neck primary.[3] Herein, we report a case of SCC occurring in the cavernous sinus, 13 years after complete excision of an EC at the same site, after ruling out known primary anywhere else in the body.

Case History

A 40-year-old woman presented with left-sided headache, diplopia, and drooping of the left eye for the past 15 days and was found to have oculomotor nerve palsy. Magnetic resonance imaging (MRI) of the brain revealed a 15 × 14 × 11 mm mass with diffusion restriction in the left cavernous sinus suggestive of an EC with a 25 × 25 × 24 mm nonenhancing solid component ([Fig. 1]). She had a history of similar complaints 13 years ago when she was diagnosed with EC at the same site. She underwent complete excision and its histopathology confirmed an EC, showing benign stratified squamous epithelial lining, abundant lamellated keratin, and foreign body giant cells. The present excision revealed an SCC composed of atypical squamous epithelial cells arranged in trabeculae and papillae ([Fig. 2A]). Cells showed abundant cytoplasmic keratinization ([Fig. 2B]) with hyperchromatic and pleomorphic nuclei. Mitoses were brisk ([Fig. 2C]). The foci of necrosis were noted ([Fig. 2D]). There was no other primary on clinical examination and imaging. The patient was then referred for radiotherapy but did not take the same and expired 1 year after the operation.

Fig. 1 A 40-year-old woman with squamous cell carcinoma in the cavernous sinus presented with headache, diplopia, and drooping of the left eye. Axial T2 and diffusion weighted magnetic resonance imaging showed a mass lesion measuring 15 × 14 × 11 mm with diffusion restriction (red arrow).

Fig. 2 (A) Atypical squamous cells arranged in trabeculae and papillae (×40, hematoxylin and eosin [H&E] stain). (B) Cells showing abundant cytoplasmic keratinization (×400, H&E). (C) Cells showing pleomorphic nuclei, prominent nucleoli, and brisk mitosis (×400, H&E). (D) Tumor with necrosis (×100, H&E).

Discussion

ECs are benign, lined by stratified squamous epithelium and contain abundant keratin with variable amount of chronic inflammation. Among intracranial locations, the cavernous sinus is a rare site. In 2018, Zhou et al published the largest case series of 31 cases of ECs of the cavernous sinus. According the study, most of them were located in the parasellar region in the middle cranial fossa with a mean age of occurrence at 46 years.[2]

Malignant transformation of benign cyst was predominant in males.[4] ECs in the cavernous sinus generally present with facial numbness, absent corneal reflex, temporal muscle atrophy, and trigeminal neuralgia followed by abducens or oculomotor nerve deficits such as diplopia.[2] Our case had a similar presentation.

Malignant transformation of EC was first described by Ernst in 1912[5] at the CPA. The largest review of literature was published in 2012 by Nagasawa et al,[1] who reviewed a total of 58 cases of malignant transformation in intracranial EC. The most frequently involved site was the CPA, but no case was seen in the cavernous sinus.[1] To date, 85 cases of SCC occurring in the EC have been reported ([Table 1]).

Table 1 Literature review of SCCs arising in intracranial ECs from 1912 to date

Sl. no.	Year	Study	Age (y)	Sex	Location	Time to progression
1	1912	Ernst et al[5]	52	M	CPA	–
2	1942	Hug et al[8]	42	M	CPA	–
3	1951	Henkel et al[9]	49	M	CPA	–
4	1955	Yamanaka et al[10]	57	M	Base of brain	4 mo
5	1960	Davidson and Small et al[11]	46	M	Frontal	3 mo
6	1960	Landers and Danielski et al[12]	73	F	Frontal	1 mo
7	1964	Komjatszegi et al	45	F	CPA	–
8	1965	Fox et al[13]	43	M	Temporal	7 y
9	1965	Toglia et al[14]	54	M	Base of brain	1 y
10	1977	Koempf and Menges et al[15]	57	F	Parapontine	–
11	1981	Dubois et al[16]	53	M	Fourth ventricle	4 mo
12	1982	Takado et al[17]	53	F	Parapontine	–
13	1983	Lewis et al[18]	53	F	Parasellar	3 y
14	1984	Bondeson and Falt et al[19]	56	F	CPA	–
15	1984	Giangaspero et al[20]	45	M	Parieto-occipital	–
16	1986	Maffazzoni et al[21]	45	M	Fronto-basal	–
17	1986	Kubokura et al[22]	60	F	Temporal	–
18	1987	Salazar et al[23]	49	M	CPA	–
19	1987	Matsuno et al[24]	43	M	CPA	1 y
20	1987	Goldman and Gandy[25]	59	F	Intraventricular	33 y
21	1988	Ishimatsu et al[26]	40	M	CPA	–
22	1989	Nishiura et al[27]	38	M	CPA	–
23	1989	Michenet et al[28]	40	M	Latero-peduncular	–
24	1989	Abramson et al[29]	37	M	CPA	–
25	1990	Gi et al[30]	39	M	CPA	1 y
26	1991	Knorr et al[31]	74	M	CPA	31 y
27	1991	Tognetti et al[32]	67	F	Temporal lobe	31 y
28	1992	Delangre et al[33]	71	F	CPA	–
29	1993	Acciarri et al[34]	62	M	Parasellar	–
30	1994	Radhakrishnan et al[35]	53	M	Frontal	31 y
31	1995	Fuse et al[36]	74	F	CPA	−
32	1995	Nishio et al[37]	57	M	CPA	1 y
33	1995	Uchino et al[38]	57	M	CPA	1.5 y
34	1995	Mori et al[39]	42	M	CPA	3 mo
35	1996	Bayindir et al[40]	67	F	Intraventricular	8 mo
36	1996	Mohanty et al[41]	20	M	Posterior fossa	–
37	1999	Murase et al[42]	50	F	CPA	12 y
38	2000	Ishikawa et al[43]	65	M	CPA	–
39	2000	Sawan et al[44]	66	M	Prepontine	–
40	2001	Asahi et al[45]	55	F	CPA	13 y
41	2001	Khan et al[46]	53	M	Prepontine	6 mo
42	2001	Nawashiro et al[47]	46	M	Temporal lobe	–
43	2002	Link et al[48]	57	F	CPA	11 y
44	2002	Hatem et al[49]	40	M	Frontotemporal	–
45	2003	Akar et al[50]	−	F	CPA	1.5 y
46	2003	Monaco et al[51]	36	M	Cisterna magna	6 mo
47	2003	Hamlat et al[4]	54	F	Temporal lobe	3 y
48	2003	Shirabe et al[52]	49	F	Ventral pons	1.5 y
49	2004	Guan et al[53]	42	F	Temporal	17 y
50	2005	Michael et al[54]	45	M	Prepontine	1 mo
51	2006	Kodama et al[55]	67	M	CPA	8 y
52	2006	Tamura et al[6]	56	F	CPA	13 y
53	2006	Ge et al[56]	50	M	Temporal	6 y
54	2007	Pagni et al[57]	65	F	Pineal region	1 mo
55	2007	Agarwal et al[58]	45	M	Posterior fossa	1 mo
56	2008	Kim et al[59]	72	F	CPA	–
57	2008	Hao et al[60]	61	F	CPA	6 y
58	2009	Ge et al[61]	44	M	Right temporal lobe	6 y
59	2010	Nakao et al[62]	74	F	CPA	20 y
60	2010	Kano et al[63]	64	F	Parapontine	16 y
61	2010	Hao et al[64]	61	F	Right CPA	6 y
62	2011	Lakhdar et al[65]	52	M	CPA	6 y
63	2012	Chon et al[66]	43	M	CPA	27 y
64	2014	Vellutini et al[67]	43	F	CPA	24 y
65	2016	Solanki et al[68]	47	F	CPA	36 y
66	2016	Pikis et al[69]	77	M	CPA	12 y
67	2017	Ozutemiz et al[70]	64	M	Lat ventricle	23 y
68	2017	Mascarenhas et al[71]	35	F	CPA	5 y
69	2018	Kwon et al[72]	35	M	Left CPA	–
70	2019	Cuoco et al[3]	71	M	CPA	40 y
71	2019	Demuth et al[73]	67	F	CPA	–
72	2019	Fereydonyan et al[74]	30	M	CPA	5 y
73	2019	Gerges et al[75]	65	F	Pineal	–
74	2020	Romesberg et al	52	M	Left CPA	6 mo
75	2021	Zuo et al[76]	39	M	CPA	–
76			54	F	Suprasellar	–
77			43	M	CPA	–
78			44	M	CPA	3 y
79			51	M	CPA	–
80			48	M	CPA	15 y
81			61	M	CPA	28 y
82			61	M	CPA	–
83			60	M	CPA	5 y
84	2021	Sakamoto et al[77]	59	F	Right CPA	6 y
85	2023	Zhang et al[78]	58	M	Right frontoparietal lobe	–

Abbreviations: CPA, cerebellopontine angle; EC, epidermoid cyst; F, female; M, male; SCC, squamous cell carcinoma.

No case of malignant transformation in EC has been reported in the cavernous sinus, thus making this the first report of such transformation.

The mechanism of malignant transformation has not been well known, but certain hypotheses suggest that subtotal resection of the cyst wall or chronic inflammation from ruptured cyst contents or introduction of foreign material intraoperatively leads to metaplasia and carcinoma.[1] [4] Malignant transformation may present itself at the initial presentation or may develop following a variable lag period of 3months to 33 years after resection of the previous benign cyst.[6]

Garcia's criteria for malignant transformation state that the tumor must be restricted to the intracranial, intradural compartment without extension beyond the dura or cranial bones and there should not be any invasion or extension through intracranial orifices. There should be no communication with the middle ear, air sinuses, sella turcica, and no evidence of nasopharyngeal tumor. Hamlat et al proposed additional criteria of the presence of benign squamous epithelium within the malignant tumor and the need for ruling out metastases.[7]

ECs are totally resected by an extradural/interdural approach as it causes less chances of brain or cranial nerve injury, but often, complete capsule removal cannot be achieved and postoperative complications such as chemical meningitis and seizures due to chemical irritation are known to occur. For intracranial SCCs, adjuvant radiotherapy and chemotherapy have proven to improve survival.[1] [2]

Our patient underwent a left temporal craniotomy and total excision. Radiotherapy was advised, but she did not take the same and expired 1 year after the operation.

Conclusion

Malignant transformation of an EC is a rare event with dismal prognosis. This is the first case of an EC of the cavernous sinus to undergo malignant transformation to SCC after 13 years of primary resection. Clinically, rapid deterioration postexcision without hydrocephalus, recurrence, or failure to recover following surgery for a benign cyst along with contrast-enhanced computed tomography or MRI findings of the lesion should raise the suspicion for malignant transformation.

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