Squamous Cell Carcinoma

ICD-O:8070/3

Squamous cell carcinoma is uncommon in the middle ear. It sometimes accompanies squamous cell carcinoma of the external canal or may arise solely from the middle ear epithelium. The patient always has an aural discharge and conductive hearing loss. Pain in the ear, bleeding and facial palsy are common.

Fig. 8.15. Microsliced specimen of jugular paraganglioma removed at autopsy. Two slices of the temporal bone in the region of the neoplasm are seen. The one on the left shows invasion of the temporal bone by the reddish paraganglioma from its apical region as far as the tympanic membrane. The slice on the right is taken at a higher level and shows sparing of the cochlea and bony labyrinth by the tumour

Fig. 8.15. Microsliced specimen of jugular paraganglioma removed at autopsy. Two slices of the temporal bone in the region of the neoplasm are seen. The one on the left shows invasion of the temporal bone by the reddish paraganglioma from its apical region as far as the tympanic membrane. The slice on the right is taken at a higher level and shows sparing of the cochlea and bony labyrinth by the tumour

Fig. 8.16. Jugular paraganglioma. The cells form small clusters, each surrounded by a row of flattened cells, probably sustentacu-lar cells, and separated by blood vessels

In microscopic sections the tumour may be seen arising from surface stratified squamous epithelium, itself metaplastic from the normal cubical epithelium. In certain areas an origin directly from basal layers of cubical or columnar epithelium may be seen. There is no evidence that the epidermoid formation, a cell rest that occurs normally in the middle ear during development (see above), may be a source of squamous cell carcinoma. The neoplasm is squamous cell carcinoma with variable degrees of differentiation. Atypical change and even carcinoma in situ may be seen in some parts of the middle ear epithelium adjacent to the growth. The mode of spread of the neoplasm from the middle ear epithelium has been ascertained in temporal bone autopsy sections [70] and this pattern has been confirmed by imaging in living patients. The carcinoma tends to grow into and erode the thin bony plate that separates the me dial wall of the middle ear, at its junction with the Eu-stachian tube, from the carotid canal. This bony wall is normally up to 1 mm in thickness and may be recognised radiologically. Having reached the carotid canal the growth will extend rapidly along the sympathetic nerves and the tumour is then impossible to eradicate surgically. Another important method of spread is through the bony walls of the posterior mastoid air cells to the dura of the posterior surface of the temporal bone. From there it spreads medially, enters the internal auditory meatus and may then invade the cochlea and vestibule. Spread into the lamellar bone in both of these situations is along vascular channels between bone trabecu-lae. A similar type of bone invasion may also occur from other parts of the middle ear surface such as in the region of the facial nerve. The special bone of the otic capsule is, on the other hand, peculiarly resistant to direct spread of growth from tumours within the middle ear, and even the round window membrane is not invaded. When invasion does occur it takes place after entry of the tumour into the internal auditory meatus and penetration of the bone by way of the filaments of the vestibular and cochlear divisions of the eighth nerve. In the later stages tumour grows extensively in the middle cranial fossa; it may also invade the condyle of the mandible. Death is usually due to direct intracranial extension. Lymph node metastasis is unusual and spread by the bloodstream even more so [70].

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