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British Journal of Radiology 75 (2002),85-86 © 2002 The British Institute of Radiology

Case of the month

A hearing problem with a difference

I Zammit–Maempel, FRCR1, I G Hide, FRCR1 and J Hill, FRCS2

Departments of 1Radiology and 2Otolaryngology, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK


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A 68-year-old man was referred to the ENT department because of right-sided hearing loss, excessive snoring, blocked nose and epiphora. On examination he was found to have a non-functioning right ear, a mild right facial palsy, hypoasthesia of the right side of his face and tongue, and multiple polyps in his left nasal cavity. In view of his deafness, he was referred forMRI of his internal auditory meati. What abnormalities are demonstrated on MRI (Figures 1–3GoGoGo)? What is the differential diagnosis and what further imaging may be helpful?



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Figure 1. T2 weighted axial image.

 


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Figure 2. T1 weighted coronal image (a) before and (b) after iv gadolinium.

 


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Figure 3. T1 weighted axial image after iv gadolinium.

 

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MRI did not demonstrate an acoustic neuroma but showed extensive irregularly enhancing tissue within the right cerebellopontine angle, nasal cavity, left ethmoidal air cells, sphenoid sinus and skull base. Abnormal enhancement extended along the right seventh and eight cranial nerves into the internal auditory canal as well as along Meckel's cave and the right cavernous sinus to engulf the internal carotid artery. CT of the sinuses and skull base confirmed slightly opacified sinuses but also showed a destructive lesion affecting the skull base (Figure 4Go) and petrous apex. The differential diagnosis at this stage was an aggressive nasal cavity/skull base tumour, including lymphoma, chordoma and chondrosarcoma, as well as aggressive inflammatory diseases such as fungal infection and extensive polyposis. The patient underwent post-nasal space examination and multiple biopsies on three separate occasions. Histology showed only inflammatory nasal polyps with reactive bone formation and fibrosis but no evidence of malignancy. The diagnosis was that of aggressive polyposis masquerading as skull base malignancy. Unfortunately this was too extensive for surgery and was treated with high dose steroids and radiotherapy.



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Figure 4. 2 mm axial unenhanced CT through the skull base showing a destructive lesion involving the clivus, sphenoid sinus and left ethmoidal air cells.

 
Nasal polyposis is a very common sinonasal problem. It is said to occur in 1.3% of the total population and in 23.4% of patients with chronic rhinitis [1]. It is generally a benign process and isusually amenable to surgical and medical treatment. The most common symptoms and signs of nasal polyposis are nasal obstruction and rhinorrhoea. Its pathogenesis is commonly considered to be related to allergy or inflammation. Although polyps are histologically benign lesions, aggressive clinical behaviour leading to bone destruction or cranial nerve compression is occasionally seen [24].

Parker et al [5] described three cases of histologically benign inflammatory sinonasal polyps acting in an aggressive manner. These were shown on CT to erode bone and invade the orbit, pterygomaxillary space and anterior cranial fossa. The authors coined the term "aggressive sinonasal polyposis". Som et al [1] argue that if bone destruction occurs in a non-sinus-bearing part of the skull base, such as the floors of the anterior and middle cranial fossae, then the destruction may be due to benign disease. This is presumably because the bones of the skull base have a more limited response to pressure than do facial bones.

Cranial nerve involvement is not that uncommon in chronic sinus disease. Weisberger and Dedo [6] noted that 4% of 122 patients with chronic inflammatory sinus disease had cranial neuropathy. Cranial nerve involvement is most frequent with sphenoid sinus polypoid disease because of its close anatomical relationship to theorbital apex. The optic nerve is the most frequently involved cranial nerve in sinus disease because of its medial location at the orbital apex, being separated from the sphenoid and posterior ethmoidal cells by only a slither of bone. The sixth nerve can also be affected because it is also relatively medially placed. Fifth, seventh, eight and twelfth cranial nerve involvement, as seen in our case, is rare.

Received for publication November 17, 2000. Accepted for publication November 27, 2000.


    References
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 Introduction
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 References
 

  1. Som PM, Lawson W, Lidov MW. Simulated aggressive skull base erosion in response to benign sinonasal disease. Radiology 1991;180:755–9.[Abstract/Free Full Text]
  2. Rejowski JE, Caldarelli DD, Campanella RS, Penn RD. Nasal polyps causing bone destruction and blindness. Otolaryngol Head Neck Surg 1982;90:505–6.[Medline]
  3. Winestock DP, Bartlett PC, Sondheimer FK. Benign nasal polyps causing bone destruction in the nasal cavity and paranasal sinuses. Laryngoscope 1978;88:675–9.[Medline]
  4. Hao SP, Chang CN, Chen HC. Transbasal nasal polyposis masquerading as a skull base malignancy. Otolaryngol Head Neck Surg 1996;115:556–9.[Medline]
  5. Parker GS, Tami TA, Wilson JF. Aggressive sinonasal polyposis. Am J Rhin 1988;2:1–5.
  6. Weisberger EC, Dedo HH. Cranial neuropathies in sinus disease. Laryngoscope 1977;87:357–63.[Medline]




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