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Limitations of Magnetic Resonance Imaging in the Evaluation of Perineural Tumor Spread Causing Facial Nerve Paralysis

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Limitations of Magnetic Resonance Imaging in the Evaluation of Perineural Tumor Spread Causing Facial Nerve Paralysis ORIGINAL ARTICLE Limitations of Magnetic Resonance Imaging in the Evaluation of Perineural Tumor Spread Causing Facial Nerve Paralysis Markus Jungehuelsing, MD; Christian Sittel, MD; Roman Fischbach, MD; Mathias Wagner, MD; Eberhard Stennert, MD Objective: To present and discuss the clinical presen- patients, the initially performed MRI did not detect any tation and treatment in patients with long-duration uni- parotid gland lesion causing the paralysis, whereas long lateral facial paralysis and normal magnetic resonance im- duration of the paralysis and electroneurography indi- aging (MRI) findings. cated malignancy. Design: Case series. Results: Exploration surgery was performed as total pa- rotidectomy in these 8 patients and malignant parotid Setting: Ear, nose, and throat department of the Uni- gland tumors were proved in all 8 patients. versity of Cologne, Cologne, Germany. Conclusions: Individuals with facial nerve paralysis Patients: A total of 486 patients with unilateral facial without any signs of regeneration 6 months after the paralysis who were treated from 1986 to 1998. Besides onset of paralysis and/or persistent electrophysiological the usual diagnostic workup, a complete electrophysi- evidence of ongoing neuronal degeneration should ological evaluation, including investigations such as needle undergo surgical exploration of the parotid gland and electromyography and neuromyography (also known as facial nerve, even if MRI studies show no tumoral electroneurography), of the facial nerve was performed lesion. at repeated intervals. In 19 patients, a malignant tumor was delineated with ultrasonography or MRI. In 8 of these Arch Otolaryngol Head Neck Surg. 2000;126:506-510 ELL PALSY, by definition, is a sion is generally considered an ominous diagnosis of exclusion. sign, almost uniformly heralding malig- Eighty percent of all periph- nant disease. Usually, tumors are pal- eral facial paralyses are la- pable and detectable using ultrasonogra- beled as idiopathic or Bell phy, computed tomography, or magnetic palsy and a complete recovery occurs in resonance imaging (MRI).3 Nevertheless, B 1 70% of all patients. it is known that computed tomography Conversely, approximately 20% of and ultrasonography may fail to depict these facial palsies can be demonstrated to small parotid gland lesions, especially if have a specific cause. All patients exhib- they are located in the deep, retroman- iting facial paralysis thus should undergo dibular portion of the parotid gland or a thorough neurotologic evaluation to close to the stylomastoid foramen.4,5 Mag- identify the underlying abnormality. netic resonance imaging has higher accu- Facial paralysis of neoplastic origin racy in identifying soft tissue lesions. With is uncommon. It is estimated to repre- its high soft tissue definition, even very sent the etiology in approximately 5% of small lesions of the parotid gland and the From the Departments of all cases.2 Neoplastic involvement may be facial nerve become identifiable, as well as Otorhinolaryngology–Head and by neurogenic primary lesions of the sev- the deep portion of the parotid gland and Neck Surgery enth cranial nerve or by secondary, ex- the intramastoid, tympanic, and labyrin- (Drs Jungehuelsing, Sittel, and trinsic neoplasms. thine sections of the facial nerve.6-9 Stennert), Diagnostic and Interventional Radiology Parotid gland disease must be ac- The purpose of this article was to pre- (Dr Fischbach), and Pathology knowledged as a significant clinicopatho- sent a series of cases of facial paralyses (Dr Wagner), University of logic entity in the pathogenesis of facial caused by malignant parotid tumors, which Cologne Medical School, paralysis. The presentation of facial pa- had not been identified by gadolinium- Cologne, Germany. ralysis in the presence of parotid gland le- enhanced MRI. (REPRINTED) ARCH OTOLARYNGOL HEAD NECK SURG/ VOL 126, APR 2000 WWW.ARCHOTO.COM 506 ©2000 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Table 1. Diagnoses and Nerve Function in Patients PATIENTS AND METHODS With Unilateral Facial Paralysis No. (%) of From 1986 to 1998, we treated in our outpatient clinic Patients Facial Nerve Function 486 patients with peripheral, unilateral facial paraly- (N = 486) Diagnosis After 6 mo* sis. In addition to the usual neurotologic investiga- 344 (71) Idiopathic (“Bell palsy”) Recovery tions (standard pure tone and speech audiometry, im- 22 (4) Herpes zoster (IgM) Recovery pedance audiometry, modified Short Increment 37 (8) Pontine angle tumor Mixed, degeneration and Sensitivity Index, Carhart tests, brainstem audiom- regeneration etry in cases of equivocal findings, Schirmer tear test, 11 (2) Any central dysfunction† No recovery, denervation stapedial reflex testing, and taste evaluation), we per- potentials formed ultrasound of the parotid gland. A complete 27 (6) Malignant parotid gland No recovery, denervation electrophysiological workup including needle elec- tumor potentials tromyography and neuromyography (also known as 0 Benign parotid gland No paralysis electroneurography) was performed at repeated in- tumor 45 (9) Trauma Depending on extent of tervals. As a routine, all patients were submitted to trauma these investigations at the time of first contact with our department, then follow-up visits were sched- *Electromyographic findings. uled 2, 6, and 12 weeks after onset of paralysis. In †Central dysfunction includes apoplectic insult, hemorrhage, and other cases of persistent paralysis with or without electro- central nervous system disorders proved unequivocally by computed physiological signs of neuronal degeneration (ie, posi- tomography or magnetic resonance imaging. tive sharp waves in needle electromyography) fol- low-up was continued at 4-week intervals. In 344 and neck coil and high-resolution MRI reconstruction. patients (76%) any specific cause of the paralysis was In 5 patients, the repeated Gd-DTPA–enhanced MRI did ruled out and the paralysis was labeled as idio- pathic. The other patients showed specific lesions as not depict any pathologic alteration. described in Table 1. In 27 patients (6%) a unilat- All 8 patients underwent total parotidectomy for di- eral facial paralysis was the first symptom of a ma- agnostic and therapeutic reasons. Histopathological in- lignant tumor of the parotid gland. Eight of these pa- vestigations revealed malignant tumors of the parotid tients had been referred to our service for facial gland in all 8 patients: adenoid cystic carcinoma with peri- reanimation surgery because of abnormally long du- neural spread in 4 patients, basal cell adenocarcinoma ration of complete facial nerve paralysis (Table 2). in 2 patients, mucoepidermoid carcinoma in 1 patient, In all 8 patients, previously performed gadopen- and acinic cell carcinoma in 1 patient. tetate (Gd-DTPA)–enhanced MRI of the parotid gland The MRI study did not detect the lesion in all pa- and of the pontine angle region had not shown any tients with adenoid cystic carcinoma and in 1 patient with pathological change, destruction, or lesion. In these 8 patients we performed, in addition to the neuroto- mucoepidermoid carcinoma. Histopathological studies logic examination and electromyography, another revealed predominant perineural, intraneural, and peri- Gd-DTPA–enhanced MRI and exploration surgery. vascular spread of the cancer without a real circum- script tumor (Figure 2). In 1 patient with basal cell adenocarcinoma, the ini- tially performed MRI did only depict an accompanying RESULTS mastoiditis, but not the tumor itself. A second high- resolution Gd-DTPA–enhanced MRI scan hinted at the Our subgroup of 8 patients showed no electrophysi- parotid gland tumor; perhaps the histological results ologic regeneration after more than 6 months of paralysis proved very low mitotic activity and subsequently the slow (range, 6-36 months; mean, 17.6 months; Table 2). After growth of the tumor may have affected the documented electromyographic diagnosis indicated neoplastic inva- MRI signal intensity similarly (Figure 3). In the re- sion, another Gd-DTPA–enhanced MRI of the cerebello- maining 2 patients, the initial MRI studies simply did not pontine angle and the parotid gland was performed in pa- cover the parotid gland lesion. In these patients the MRI tients in whom MRI studies did not cover the whole parotid studies were performed primarily to exclude a cerebel- gland or in whom MRI studies had low diagnostic qual- lopontine angle tumor, but later served as guarantee for ity. Electromyographic criteria for neoplastic invasion were safe tumor exclusion. pathological spontaneous activities without interference activity pattern or intermediate activity pattern, but some- COMMENT times with transitory single oscillations in patients with clinically complete facial paralysis. Delineation of circumscribed tumoral lesions of the pa- In 2 patients a parotid gland tumor was diagnosed rotid gland today is the domain of ultrasonography, and, immediately (Figure 1). The formerly performed MRI for the deeper portions of the parotid gland, of MRI. Es- studies had simply not covered the parotid gland lesion, pecially for the evaluation of tumors of the stylomastoid but only the cerebellopontine angle region for acoustic foramen and the retromandibular part of the parotid gland, neuroma exclusion and the upper parts of the parotid MRI is the method of choice.6-10 gland. In 1 patient, tumoral invasion of the deep por- Magnetic resonance imaging
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