May [5] listed 81 distinct causes of peripheral facial nerve palsies, including traumatic, infectious, and metabolic. Idiopathic Bell palsy accounted for 57% of the 1575 cases he himself reported. Peripheral facial nerve palsy is associated with nonmalignant parotitis. Andrews and colleagues [6] found only 10 reported cases and presented three more. Our extensive MEDLINE search failed to reveal any previously reported associations between facial nerve palsy and radioiodine treatment. We present two cases of facial nerve palsies in patients who developed parotitis after radioiodine therapy.

View larger version (107K): [in this window] [in a new window]   Figure 1. Diagnostic and post-therapy radioiodine scans. Twenty-four-hour scans after the diagnostic (74 MBq or 2 mCi) dose (top) and post-therapy scans (bottom). Note the intense uptake in the region of the parotids in patient 1 (left) compared with the more moderate uptake in patient 2 (right).

Case Reports

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A 51-year-old man had locally invasive (stage 2) papillary thyroid carcinoma, for which he was treated with a thyroidectomy with lymph node dissection. Nineteen years later, he had a second operation for recurrent disease, which was followed by 1070 MBq (29 mCi) of iodine-131.

One year later, he had a radioiodine dosimetry with a thyroid-stimulating hormone of 134 mU/L. The 24-hour thyroid bed and right and left parotid gland uptakes were 2.4%, 9.6%, and 6.9%, respectively. When we retrospectively analyzed the available data points, using Medical Internal Radiation Dose techniques [7], we estimated that the radiation dose delivered with 9620 MBq (260 mCi) to the recurrent thyroid cancer, the right and left parotid glands, and the blood were 112 000, 21 000, 13 500, and 200 rad, respectively.

The patient developed severe sialoadenitis with marked engorgement and tenderness of the parotids within 24 hours and lost taste sensation 3 to 4 days later. After 9 days, he developed a partial right peripheral facial nerve palsy and was treated with a 5-day course of prednisone. A magnetic resonance imaging scan of the face showed no abnormalities. At 3 months' follow-up, he had nearly total recovery of facial nerve function but had persistent xerostomia.

Patient 2

A 60-year-old man had locally invasive (stage 2) papillary thyroid carcinoma. He had a total thyroidectomy with modified neck dissection and two subsequent neck revisions for recurrent disease during the next 5 years. Iodine-131 dosimetry, done when his thyroid-stimulating hormone was 93 mU/L, showed residual tumor. Twenty-four-hour neck and right and left parotid gland uptakes were 2.1%, 0.5%, and 0.4%, respectively. With a 13 690 MBq (370 mCi) dose, the estimated radiation dose delivered to the thyroid cancer, the parotid glands, and the blood were 13 400, 2200, 1500, and 200 rad, respectively. He had only mild midline neck and parotid tenderness. However, 10 days later, he developed a right peripheral facial nerve palsy. No specific treatment was given, and the patient had nearly total resolution during the next few months.

Discussion

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Bell palsy is common, especially in the third to fifth decades of life. The comorbidity of facial nerve palsy in our patients could have been merely chance. However, the compelling temporal relations suggest otherwise. Earll and Kolb [8] described two cases of facial paralysis occurring with severe myxedema. Operative findings in one of his patients suggested that the cause was increased pressure on the seventh cranial nerve within the facial canal. Cox described another patient whose "idiopathic" Bell palsy failed to resolve until the previously unrecognized hypothyroidism was treated [9]. The duration of frank hypothyroidism in our patients was only 2 to 3 weeks, and they had been restarted on thyroxine for at least 1 week. Nonetheless, myxedema may have contributed to the compression of the facial nerve.

The first patient lost taste sensation. Rarely, patients with Bell palsy report an alteration in taste sensation, which is thought to represent concurrent inflammation of the chorda tympani. Alteration in taste is a common complaint in patients having radioiodine treatment. The exact mechanism is uncertain, but decreased saliva production and altered composition have been proposed. Typically, the chorda tympani branches separate from the facial nerve 4 mm proximal to the stylomastoid foramen. Thus, it is unlikely that parotitis should involve the chorda tympani.

Inflammation involving the facial nerve could have caused the development of the paralyses in our patients. Lee described the development of vocal cord paralysis after radioiodine therapy and postulated that it was caused by local inflammation [10]. However, the onset of weakness occurred at least a week after the peak inflammation and several days after the clinical resolution of parotitis. Further, the patients differed in the degree of salivary gland uptake and clinical sialoadenitis (Figure 1). Neither patient had clinical evidence of tumor infiltration of the parotid glands.

Another possible explanation is direct radiation injury to the facial nerve. The ß radiation from iodine-131 penetrates approximately 2 to 3 mm. Thus, highly concentrating parotid tissue surrounding a strategic point along the nerve or vaso nervosum could have caused sufficient damage.

Conclusion

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Peripheral facial nerve palsy developed after high-dose radioiodine treatment in two patients. Possible causes include coincidental Bell palsy, parotitis, myxedematous changes, or direct radiation effect.