Two 1.5-T signa units, software levels from 4.8 to 5.2 (General Electric, Milwaukee, Wis) were used. Either a quadrature head coil or a receive-only volume cervical coil was used. Images were obtained in 5-mm-thick sections with 1-mm intersection gap. T1-weighted imaging param- eters were 550-650/10-15/1 (repetition time/echo time/ excitations), with 256 3 192 matrix. T2-weighted imaging parameters on spin-echo sequences were 2000-2500/20- 80/0.75-1, superior and inferior saturation pulses, with 256 3 192 matrix. T2-weighted imaging parameters on fast spin echo sequences were 5000-6000/119 (effec- tive)/2-4; echo train length, 119; single echo, superior, and inferior saturation pulses; image matrix varying from 256 3 192 to 512 3 256. Fat suppression in FS FSE T2 and in most gadolinium-enhanced images was achieved by the frequency-selective, chemical-presaturation method. The other fat-suppressed T2-weighted sequence was IR FSE T2, with the parameters 4000-6000/26-85/1; 256 3 192 matrix; and 140 to 170 inversion time. For all images, window/level settings were carefully adjusted by experienced MR imaging technologists to optimize tissue contrast in the parotid space.
PURPOSE: To compare cardiac-triggered dual-echo spin-echo and magnetization transfer–pre- pared gradient-echo (MT-GE) MR imaging in the detection of multiple sclerosis (MS) lesions in the spinal cord. METHODS: The cervical spinal cord in 20 patients with MS and in nine healthy volunteers was examined with spin-echo and MT-GE MR imaging. Sagittal images were scored for number of lesions, certainty about lesions, image quality, and visual hindrance by artifacts in random order by two radiologists separately and in a blinded manner. RESULTS: In one healthy volunteer, a lesion was seen on images obtained with both images. Lesion/cord contrast-to-noise ratio was equal on both the MT-GE and T2-weighted spin-echo images. MT-GE images showed better image quality and fewer artifacts than the spin-echo images did. The readers found approx- imately the same number of lesions. However, the number of definite lesions was higher for the spin-echo sequence than for the MT-GE sequence. One reader found 45 definite lesions with spin-echo and 34 definite lesions with MT-GE. For the other reader, these numbers were 37 (spin-echo) and 31 (MT-GE). On the spin-echo images, 90% of the patients were considered to have definite lesions; on the MT-GE images, the readers found definite lesions in 65% (reader 1) and in 70% (reader 2) of the patients. CONCLUSION: Image quality was better with the MT-GE technique than with the spin-echo technique, and lesion/cord contrast-to-noise ratio on the MT-GE images was equal to that of T2-weighted spin-echo images. However, for detecting spinal cord MS lesions in the sagittal plane, the spin-echo images were preferred to the MT-GE images.
ber of lesions. Since there were obvious contrast differences, the observers could not be blinded to the type of sequence. At stage 1, each of the sequences from each subject was evaluated randomly, and lesions were marked on the hard copies. At this stage, the observers did not know to whom the images be- longed. When the MT-GE images were considered, both im- ages (ie, with and without the MT pulse) were viewed side- by-side in order to increase confidence in lesion identification. At stage 2 of image analysis, which occurred 1 month after stage 1 was completed, the two observers met again and re- viewed all sequences from the same subject simultaneously in order to clarify the reasons for any differences in the sensitiv- ities of the three sequences. In addition, ghost artifacts from subject motion or CSF flow, and truncation-type artifacts were classified as absent, not affecting or reducing the confidence of the reading. During this second review, a retrospective count of lesions was performed for each sequence: when the observ- ers agreed that a lesion not previously seen on one of the three sequences could be identified using the information from one or both of the other two, this lesion was added to the count. Conversely, when a hyperintense area, which was counted as a lesion at stage 1, was, on reflection, considered not to be a lesion using the information coming from the other sequences, it was removed from the previous count. The reasons that might explain these discrepancies were recorded. Once the le- sions were identified, they were classified according to their location in the cervical cord and their length relative to the spacing of the vertebral bodies. They were also classified as lesions that either occupied or did not occupy the entire cord cross-sectional area; the latter were then divided into mainly anterior, central, or posterior lesions. It was also noted whether the cord morphology was altered by the presence of lesions (ie, whether there was cord swelling or atrophy). Using con- trast-enhanced T1-weighted images, the lesions that appeared hypointense or enhancing were also counted.
This prospective study was done on 100 cases who underwent MRI knee,in which FSPD A Pilot study of 10 normal (young asymptomatic)subjects was done initially to define range and mean of normal values and artifacts. A sub study of 15 cases was also done comparing FSPD images, T2* maps with arthroscopy, to determine relative accuracy of either technique against the gold standard of arthroscopy. Clinical history of patients was taken before examination. MRI was performed with a Siemens AvantoMagnetom 1.5 TESLA MR only knee coils. The patient was placed in the supine position with the knee placed within knee coil in neutral position. MR images were systematically obtained without administration
PURPOSE: To compare the sensitivity of conventional spin-echo, fast spin-echo, fast fluid- attenuated inversion recovery (FLAIR), and turbo gradient spin-echo MRsequences in the detec- tion of multiple sclerosis lesions. METHODS: Conventional spin-echo, fast spin-echo, fast FLAIR, and turbo gradient spin-echo sequences were performed on a 1.0-T MR imager in seven patients with clinically definite multiple sclerosis. The images in each sequence were evaluated by two raters and consensus was reached by agreement. RESULTS: In comparing conventional spin-echo with fast spin-echo sequences, five lesions were seen only by conventional spin-echo and 63 were seen only by fast spin-echo; in comparing conventional spin-echo with fast FLAIR sequences, 18 lesions were seen only by conventional spin-echo and 109 only by fast FLAIR; in comparing conventional spin-echo with turbo gradient spin-echo sequences, 51 lesions were seen only by conventional spin-echo and seven only by turbo gradient spin-echo; in comparing fast spin-echo with fast FLAIR sequences, 45 lesions were seen only by fast spin-echo and 52 only by fast FLAIR. CONCLUSION: Fast spin-echo and fast FLAIR sequences improve the sensitivity of MR imaging in the detection of multiple sclerosis lesions with reduced acquisition time as compared with con- ventional spin-echo sequences. These sequences should therefore be considered for serial studies in patients with multiple sclerosis. The sensitivity of turbo gradient spin-echo was inferior to the other sequences, but its reduced acquisition time could make this technique the ideal choice for patients who cannot tolerate longer examination times.
MR imaging was performed on 1.5 T clinical MR scanner (Magnetom Avanto, Siemens Healthcare, Erlangen, Germany) equipped with 8-channel phased array head and neck coil. A transverse SWI sequence was performed with 49 ms/40 ms (TR/TE), a field of view of 23 cm, a matrix of 256×256, a flip angle of 15°, a num- ber of averages of 1, a 2 mm section thickness, a 0.4 mm intersection gap, phase encoding direction was from R to L. Phase image, mini- mum intensity projection (MinP), and magni- tude image were reconstructed automatically by the system. Pre-saturated slabs were used to saturate contains air structures. Scanning range included neck and parotidgland zone. Imaging features including the venous distribu- tion, d v-max , ITSS, and N/S ITSS . Small vein shows contiguous low-signal regions on SWI were observed in consensus by two experienced radiologists (Dong Xie., Guanqiao Jin.; 20 and 15 years of experience in reading parotidgland Table 1. Histopathological diagnoses of parotidgland
went antibiotic therapy and had an uneventful course thereafter. No abnormal findings were noted at fol- low-up US examination, and our MR and digital sub- traction sialographic studies were unremarkable (Fig 3). Eleven glands (four parotid and seven submandib- ular) were finally found to have sialolithiasis (Fig 4). In seven patients with nonspecific pain and/or swell- ing of a salivary gland and without abnormal changes at MR sialography and digital subtraction sialogra- phy, the clinical follow-up after sialography showed no abnormal findings. In these patients, no therapy was undertaken. High-grade stenoses of the Stensen duct were diagnosed in three patients. All these stric- tures were treated with transluminal dilation. In eight further investigated glands, the final diagnosis was not attributable to the salivary duct system, but revealed parenchymal cystic lesions (n ⫽ 2), hyperplasia of the masseter muscle (n ⫽ 2), sarcoidosis (n ⫽ 2), lymph- adenitis (n ⫽ 1), and cystadenolymphoma (n ⫽ 1).
readers but still as very good. The STIR-FSE images showed some image blurring which, however, did not compromise the diagnostic efficacy even for the smallest multiple sclerosis plaques. The T2-weighted FSE-2500 images had a slightly increased image noise as com- pared with the T2-weighted FSE-3000 images, and the cerebrospinal fluid was less bright and less homogeneous on this type of image. A markedly and significantly lower overall image quality was found for the FLAIR-FSE and proton density–weighted CSE sequences but without significant differences between these two se- quences (Student-Newman-Keuls test, P , .05). Overall image quality of the T2-weighted CSE sequence was rated lowest by both readers (significant Student-Newman-Keuls test, P , .05). FLAIR-FSE images were degraded by dis- turbing artifacts from cerebrospinal fluid pulsa- tions and by image noise. On FLAIR-FSE im- ages, cerebrospinal fluid signal was not homogeneously suppressed but showed a high signal in some areas, particularly in compart- ments of the subarachnoid space with a prom- inent flow void on bright-cerebrospinal-fluid im- ages. This complicated image analysis and was thought to have reduced diagnostic efficacy in 13 cases. The flow voids on bright-cerebrospi- nal-fluid images were considered to have defi- nitely reduced the diagnostic efficacy only on the STIR-FSE images of one patient but in none of the other images. Overall image quality of CSE images was affected by pronounced image noise, while the proton density–weighted CSE images were less severely degraded than the T2-weighted CSE images. Ghost artifacts defi- nitely reduced the diagnostic efficacy of CSE images in four patients (T2-weighted CSE im- ages in four patients and proton density– weighted CSE images in three patients). Trun- cation-type artifacts were noticeable on CSE and FSE images, but were not thought to have definitely reduced the diagnostic efficacy of any image.
One radiologist (K.M.) measured the signal intensities of the lesions on each dynamic image with an electronic cursor to define the region of interest in each patient. Where markedly heterogeneous enhancement was seen, multiple regions of in- terest were obtained. Time–signal intensity curves were then plotted from signal intensity values obtained for the tumors, the ipsilateral artery, and the ipsilateral vein. Time–signal in- tensity curves were divided into five types according to those presented by Takashima et al (14): type A, curve peaks 3 to 30 seconds after administration of contrast material; type B, curve peaks at 33 to 60 seconds; type C, curve peaks at 63 to 180 seconds; type D, gradual upward slope; and type E, unen- hanced. Type C was divided into four subtypes: C1, curve peaks at 63 to 90 seconds; C2, curve peaks at 93 to 120 seconds; C3, curve peaks at 123 to 150 seconds; and C4, curve peaks at 153 to 180 seconds. Washout ratio was calculated by a modified method of that presented by Yabuuchi et al (12) as follows:
The differential diagnosis includes benign and malignant parotid tumors, especially Warthin tumors and adenoid cystic carcinomas, which may also have a solid cystic appearance. These tumors rarely occupy the total gland parenchyma. In particular, Warthin tumors are bilateral in up to 10% of cases reported. They present as well-circum- scribed, partly cystic and partly solid lesions on MRI and are often located in the tail of the parotidgland. Adenoid cystic carcinoma usually presents as an infiltrating mass with a high propensity for perineural invasion. On MRI adenoid cystic carcinoma has an irregular contour, poorly defined margins, and a strong enhancement after the administration of contrast medium .
Because of the benign nature of this lesion, ac- curate clinical and radiologic diagnosis is important so that unnecessary biopsy may be avoided (1). Any large, rapidly growing parotid mass in an in- fant, particularly if it is small or unnoticed at birth, is most likely to be HAE. HAEs are often multiple, and the diagnosis is supported, but not proved, by the presence of a cutaneous lesion (‘‘strawberry hemangioma’’), either locally (3, 5) or at a remote site (1, 5). The natural history of HAE is rapid enlargement in infancy (the proliferative phase), followed by gradual spontaneous involution, start- ing at about 8 to 18 months, and continuing until the age of 5 to 8 years (2). Significant systemic complications such as cardiac failure (6) or Kasa- bach-Merritt syndrome (7) are rare. When they oc- cur, therapy with oral corticosteroids or interferon a 2a or both may be used, although these may be less successful for parotidlesions than for hemangiomas arising at other sites (5). Surgical re- section is not recommended because of the risk of damage to the facial nerve and favorable prognosis with expectant management (3).
weighted images, with more frequent cystic change. The basal cell adenoma is sometimes mistaken for adenoid cystic carcinoma. There are two features that help to distinguish these lesions. One is the circum- scription of the basal cell adenoma, which contrasts with the invasive pattern of adenoid cystic carcinoma. The other is the lack of vascularity in the microcystic areas of adenoid cystic carcinoma, which contrasts with the numerous endothelial-lined channels in basal cell adenoma. Although basal cell adenocarcinoma is an epithelial neoplasm that has the cytological char- acteristics of basal cell adenoma (10), it is character- ized by invasive and destructive morphologic growth, in contrast to the noninvasive appearance of basal cell adenoma. Even in the multinodular forms of mem-
Summary: Purpose: The head and neck surgeon’s fascination with parotid surgery arises from the gland’s spectrum of histo- pathological presentations, as well as the diversity of its morphological features. A mass arising in the mid-cheek region may often be overlooked as a rare accessory lobe parotid neoplasm. This report serves to revisit the topic of accessory pa- rotid gland neoplasms to emphasize proper management, particularly the surgical aspects, so that consequences of saliva- ry fistula, facial nerve paralysis, and recurrence are avoided. Case report: We report a case of mucoepidermoid carcinoma which was assessed pre-operatively as arising from the accessory parotidgland of a 11-year-old female. She had complained of a painless and round mass of the left cheek for a duration of 12 months. Sialography, ultrasonography, CT scan and MRI were performed preoperatively. Sialography revealed a small duct separating from the Stensen’s duct. CT and MRI showed that the tumor with smooth outline was lying on the masseter muscle and detached from the main parotidgland. The preoperative diagnosis was an accessory parotidgland tumor. The tumor was removed without facial nerve injury via standard parotidectomy incision. The tumor was composed of mucous, intermediate and epidermoid cells. The patho- logical diagnosis was low-grade mucoepidermoid carcinoma. Conclusions: Accessory parotidgland neoplasms are rare and may present as innocuous extraparotid mid-cheek masses. A high index of suspicion, prudent diagnostic skills (including fine-needle aspiration [FNA] biopsy followed by computed tomography [CT] imaging), and scrupulous surgical approach (extended parotidectomy-style incision and limited peripheral nerve dissection when possible) are the keys to successful management of these lesions.
Solitary fibrous tumor (SFT) was described by Klemperer and Rabin in 1931 as a tumor derived from the pleura . Because of its alleged mesothelial origin, the tumor has been referred to by numerous other names (fibrous mesothelioma, localized fibrous tumor, localized mesothelioma, and benign mesothelioma), most of which are now outdated . During the same period, Stout and Murray  defined hemangioperi- cytoma (HPC) as an uncommon vascular tumor, arising from perivascular cells known as pericytes, and arranged outside the basement membrane of the capillary wall. It was postu- lated that the pericytes possessed smooth muscle cell features and, thus, were responsible for vessel caliber regulation owing to their contractile capability, modulating both flux and per- meability . It was later demonstrated that SFT is most likely derived from adult mesenchymal stem cells, and its micro- scopic architecture and immunohistochemical characteris- tics make it nearly impossible to differentiate it from HPC . Extrapleural SFTs have been reported in nearly all anatomic sites, with approximately 6% developing in the head and neck [6–8]. SFT of the parotidgland is a rare tumor; only a few cases been described in the literature [9–13]. In this paper we describe the diagnostic and therapeutic challenges of a giant parotid SFT.
Knowledge of anatomic variations concerning head and neck veins is important to surgeons performing interventions in these regions, as well as to radiologists. The retromandibular vein is used as a guide to expose the facial nerve branches inside the parotidgland, during parotid surgery and open reduction of mandibular condyle fractures. It is also used as a landmark for localisation of the nerve and compartmentalisation of parotidglandlesions preoperatively, during computed tomography, magnetic resonance imaging and sonography. In this paper, the anomalous retromandibular vein’s course on the left side of a male cadaver is described. The vein was formed around the nerve, while the maxillary vein travelled medial to the facial nerve branches and superficial to the superficial temporal vein. Interestingly, the facial nerve temporofacial division crossed again the superficial temporal vein upwards, forming a “nerve fork”. The incidence of the reported variability of the relationship between the retromandibular vein and the facial nerve are discussed with a detailed literature review. Accordingly, the typical deep position of the retromandibular vein in relation to the facial nerve is estimated to 88.17% to all sides. Furthermore, an updated classification system is proposed, including 4 types and subtypes. (Folia Morphol 2013; 72, 4: 371–375)
Well-circumscribed simple cysts without nodularity or invasive features will be of a benign or inflamma- tory etiology in most cases. Peripheral cyst enhance- ment suggests primary or secondary infectious or in- flammatory process. If associated nodularity is present, however, this should raise concern for War- thin tumor. Adjacent soft-tissue stranding can be a clue with infectious causes. Branchial cleft cyst may be difficult or impossible to differentiate from an infectious process such as nontuberculous nodal in- fection if a sinus tract or other developmental clue is not present. Either a first or second branchial cleft cyst may manifest in the parotidgland. A first branchial cleft cyst may manifest as an intraparotid cyst, sinus tract, or fistula (18). Three first branchial cysts were found in the current series, although one case was not surgically confirmed.
solitary, solid, irregular, less lobulated nodule with homogenous density, complicated by small cystic degeneration and calcification. In contrast, Secondary LEC could multiple nodules associated with cystic degeneration. Of the 7 cases of patients with primary LEC studied in the present study, 6 had homogenous densities; and small cystic degeneration and calcification occurred in 1 case each, respectively. 3) Pattern of enhancement: All of the nodular lesions were significantly enhanced. Markedly enhancement was observed in the 7 patients with primary LEC, whereas the 1 patient with secondary LEC exhibited obvious ring enhancement, the increment of CT values ranged from 33.8 to 73.4 HU. Homogeneous enhancement was acquired in 4 patients, while heterogeneous enhancement in 3 patients. 4) Margins of nodule: Most lesions had poorly- defined margins, while only a minority of lesions had well-recognized margins. In the present study, 5 lesions of LEC nodules had blurred margins whereas 2 lesions had clear margins. 5) Peripheral infiltration. Involvements of sub- mandibular vein took place in 2 cases; on the other hand, enlarged peri-glandular lymph nodes and homogenous enhancement were visualized in 2 cases. 6) Well prognosis. On 3 years of follow-ups, no metastasis and recurrence occurred in 6 patients, while 1 patient had liver and retroperitoneal lymph node metastases occurred.
Desmoid tumor is a proliferation of a mesenchymal, fibroblastic or myofibroblastic tissue. It is a non-capsulated tumor. Despite its benign nature, desmoids tumor have an aggressive behavior.Its localization in the parotidgland has rarely been reported in the literature. The particularity of this location in the head and neck is the proximity of Vascularnervous structures, the facial nerve in the parotid location and the consequence, if affected, on the facial motility especially that this tumor often occurs in young people. The clinical presentation is often about a slow- growing mass characterized by being: painless, ill-defined, firm, non-inflammatory, deeply located, and fixed to the underlying structures. Treatments strategies, always made by a multidisciplinary committee, are based on the natural biological behavior of this deep fibromatosis which is unpredictable and variable. Surgery could be undergone every time it is radical. Radiotherapy could also be played. However, the most relevant point is that actually, most authors highlighted the conservative approach by the “wait and see” policy for primary as well as for recurrence of the disease after surgical resection or radiotherapy.
A 71-year-old woman was diagnosed with follic- ular thyroid carcinoma (FTC) in the left thyroid lobe without regional lymph node metastasis 25 years ago. She was treated with left lobar subtotal thyroidectomy and ipsilateral central compartment node dissection, and received postoperative thyroid hormone suppressive therapy. Twenty-five years after the initial treat- ment, the patient presented with a slow-grow- ing, painless left parotid mass. On physical examination, a firm, immobile, 2.0×2.0 cm swelling in front of the left ear was detected, along with multiple enlarged lymph nodes at the neck, that were firm, immobile, with unclear borders, and about 0.5~2.0 cm in size. The postoperative scar could be seen in the neck, and no facial palsy was detected. The CT showed a 2.5×1.3 cm heterogeneous density in the left parotid region, metastatic malignant tumors in both lungs, and the margin of the left residual thyroid was not clear. FNAB guided by ultrasonography of the left parotid mass re- vealed that it was a salivary gland tumor in ori- gin that typically tends to be malignant. A left superficial parotidectomy, a left residual thy- roidectomy, a right thyroidectomy and a left modified radical neck dissection were perfor- med. Histologically, the left parotid lesion showed metastatic follicular carcinoma of the thyroid, and local recurrences in the left residu- al thyroid and neck lymph nodes were present. Subsequently, the patient was treated with radioactive iodine, but a pulmonary evolution appeared, and she was still alive 8 years after the left superficial parotidectomy.