CLINICAL STUDY

Preliminary Study of Diffusion-Weighted Imaging and Magnetic Resonance Spectroscopy Imaging in Kimura Disease Jie Wang, MD,* Zuohua Tang, PhD, MD,* Xiaoyuan Feng, PhD, MD,† Wenjiao Zeng, PhD, MD,‡ Weijun Tang, PhD, MD,† Lingjie Wu, MD,* and Lixin Jin, MD§ Abstract: In this study, we evaluated the value of diffusionweighted imaging (DWI) and magnetic resonance (MR) spectroscopy imaging (MRSI) combined with computed tomography (CT) and conventional MR imaging (MRI) in the diagnosis of Kimura disease (KD). The clinical data and CT and MRI findings of 5 patients with KD proven by histopathologic examination were retrospectively reviewed. Diffusion-weighted imaging and MRSI were performed at 1.5 T in 3 patients with KD. Apparent diffusion coefficient (ADC) values and the choline/creatine ratio of the lesions were compared with those of the contralateral normal parotid glands. All imaging results were compared with histopathologic findings. The typical features of KD were subcutaneous lesions, continuously infiltrative parotid lesions with or without intraparotid lymphadenopathies, and reactive cervical lymphadenopathies on CT and conventional MRI. On DWI, the ADC values of all subcutaneous and infiltrative parotid lesions were higher compared to those of normal parotid glands, and the ADC values of reactive lymphadenopathies were lower compared to both. The choline/creatine levels of subcutaneous and infiltrative parotid lesions were slightly higher than those of normal parotid glands. In conclusion, DWI and MRSI offer valuable information that may be characteristic of KD, which can highly suggest the diagnosis of KD when combined with morphological imaging.

K

imura disease (KD) is a rare benign chronic lymphoproliferative disease with unknown etiology. It typically occurs in young Asian men and frequently involves the head and neck regions, such as the salivary glands, oral cavity, and cervical lymphatic chains. Less commonly, it can occur in the axilla, groin, trunk, abdomen, and peripheral limbs.1–4 The main clinical features include painless subcutaneous soft tissue masses, regional lymph node enlargement and increased immunoglobulin E, and eosinophilia in the peripheral blood.1 Over the past few years, the roles of DWI and MRSI have been evaluated in the imaging of tumors in the head and neck region.5–11 As DWI is very sensitive to biophysical abnormalities associated with pathologic changes, even at very early stages of disease, it has been recently advocated for functional imaging of the parotid glands.5,6 Meanwhile, MRSI can provide metabolic information for tumors, and this has been shown to have potential clinical applications in the diagnosis and management of patients with brain and prostate tumors. To date, some reports of KD have been published concerning its associated radiological characteristics, including those on CT and MRI.12–16 To our knowledge, only one report using DWI to evaluate KD has been published,6 and no studies evaluating KD by MRSI are available. In this paper, we report the CT and MRI findings of 5 patients with KD and available pathologic findings. We also emphasize the value of DWI and MRSI in the diagnosis of KD in 3 patients.

Key Words: Kimura disease, CT, MRI, diffusion-weighted imaging, MR spectroscopy imaging (J Craniofac Surg 2014;25: 2147–2151)

From the *Department of Radiology, Eye & ENT Hospital of Shanghai Medical School, Fudan University, Shanghai; †Department of Radiology, Huashan Hospital of Shanghai Medical School, Fudan University, Shanghai, ‡Department of Pathology, Shanghai Medical School of Fudan University, Shanghai; and §Siemens Ltd. Healthcare Sector, Shanghai, China. Received February 7, 2014. Accepted for publication June 13, 2014. Address correspondence and reprint requests to Dr. Zuohua Tang, Department of Radiology, Eye Ear Nose & Throat Hospital, Fudan University, 83 Fenyang Rd, Shanghai, 200031, China; E-mail: [email protected] Co-corresponding author: Dr. Xiaoyuan Feng, Department of Radiology, Huashan Hospital of Shanghai Medical School, Fudan University, Shanghai, 200040, China; E-mail: [email protected] The authors report no conflicts of interest. Copyright © 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000001142

MATERIALS AND METHODS Patients Five patients (all men; mean age, 38.2 years; age range, 21– 54 years) with pathologically confirmed KD were treated in our hospital. Owing to the type of review, approval by our institutional review board was not required, and the need for patient informed consent was waived. Clinical records including patient age, sex, clinical presentation, and laboratory examinations were reviewed.

Imaging Techniques CT Examinations Computed tomographic scans were performed at 120 kV and 180 mA with a 5-mm section thickness and gap on a spiral multirow CT (Siemens SOMATOM Sensation 10) before and after intravenous injection of iopromide (Ultravist 300; Schering, Germany; 1.5 mL/kg [body weight]).

MR Imaging Magnetic resonance imaging was performed on a 1.5-T scanner (Avanto; Siemens Medical Solutions, Forchheim, Germany). Axial turbo inversion recovery magnitude, T2-weighted images

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(T2WIs), and axial and coronal T1-weighted images (T1WIs) were acquired before and after contrast medium injection (Magnevist; Bayer Schering Pharma, Berlin, Germany; 0.2 mmol/kg [body weight]). The last imaging sequence was performed after MRSI was completed. Diffusion-weighted imaging (spin-echo echo-planar imaging; repetition time/echo time, 3000/87 milliseconds [ms]; field of view, 230 mm; matrix, 128  128, thickness/gap, 5.0/0.5 mm; number of excitation, 2; b, 0, 500, and 1000 seconds/mm2, x-, y-, and z-gradient directions) was performed on the same transverse plane before contrast medium injection. The MRS slice (point resolved spectroscopy; repetition time/echo time, 1690/135 ms; field of view, 60  60  30 mm; voxel size, 3.8  3.8  30 mm3; number of excitation, 4) that crossed the largest diameter of the lesion on T2WIs was chosen, and the point resolved spectroscopy box volume was positioned on the parotid lesions. Areas of subcutaneous lipid and varying magnetic susceptibility were avoided.

Data Postprocessing and Image Analysis The location, number, morphology, margin, signal intensity/ density of MRI or CT, lesion texture, contrast enhancement patterns, and involvement of adjacent structures were reviewed for each lesion. The size and enhancement of concurrent lymphadenopathy were also evaluated. The raw DWI and MRSI data were processed offline at a workstation (Syngo; Siemens Medical Solutions) using the standard Syngo software provided by Siemens. Regions of interest (ROIs, approximately 20 mm2) were agreed upon by consensus, and care was taken not to include adjacent arteries and veins in the ROIs. For ADC measurements, the slice that crossed the largest diameter of the lesion on the ADC maps was chosen. Three ROIs were manually placed within the lesions, and the averaged ADC value was obtained. The mean ADC value of 3 ROIs in the contralateral normal parotid gland was also obtained for comparison. For each lesion, a metabolic map of the choline (Cho)/creatine (Cr) ratio was produced. The ratios of the area under the resonance peaks of Cho and Cr among the various corresponding voxels were calculated, and the results were compared with those from samples of normal parotid gland tissue.

Histopathology Surgery was performed in all cases by experienced head and neck surgeons, and most of the lesions were resected. Histopathologic sections were taken from the lesions by using direct visualization by 2 skilled pathologists. Postsurgical specimens of the lesions were fixed with 40 g/L of formaldehyde and embedded in paraffin. Five-micrometer sections taken from the greatest diameter of the lesions were prepared for hematoxylin and eosin staining.

RESULTS We examined 5 patients with KD arising in the head and neck region, which are summarized in Table 1. All patients presented with painless, slowly growing, palpable masses. Local recurrence occurred in patients 2, 3, and 4 after their first surgery in other hospitals. The diagnosis of KD was confirmed by histopathologic examination in all patients. All the subcutaneous lesions consisted of variable degrees of dense collagen fibrosis, capillary proliferation, and chronic inflammation by infiltrating lymphocytes, reactive lymphoid follicles, eosinophils, and plasma cells. The lymphadenopathies of patients 2 and 3 showed the following: prominent lymphoid follicular hyperplasia with reactive germinal centers and wellformed mantle zones; eosinophilic infiltrates in interfollicular areas, sinusoids, and perinodal soft tissue; and proliferation of postcapillary venules. The history was variable, ranging from 1 year to 17 years (mean, 7 years). In our study, all patients underwent CT and/or MRI examinations before any therapy. Of the 5 patients, 2 patients underwent CT, one underwent MRI, and the other 2 patients underwent both CT and MRI (Table 2). Furthermore, 3 patients were also examined with DWI and MRSI (Table 3).

CT and Conventional MRI The CT and MRI features of all lesions are summarized in Table 2. All patients demonstrated subcutaneous lesions; and patients 2, 3, and 4 also presented ipsilateral parotid lesions. No necrosis or cystic degeneration was observed in any patient. The greatest diameter of all lesions ranged from 1 to 8 cm, with a mean of 4.1 cm. Parotid lesions were divided into 3 types retrospectively: 1, continuously infiltrative lesion from a subcutaneous lesion; 2, enlargement of intraparotid lymphadenopathies; and 3, mixed pattern. Patient 2 had type 3 lesions, whereas patients 3 and 4 had type 1 lesions. All patients had ipsilateral cervical lymphadenopathies that were homogeneous and without necrosis; patient 3 also had contralateral cervical lymphadenopathies. The long nodal axis of the cervical lymphadenopathies ranged from 10 to 29 mm. On CT, all 4 patients showed a homogeneous, isodense area on unenhanced CT and moderate enhancement. In patients 2 and 3 (Figs. 1, 2), who had heterogeneous enhancement, multiple intense nodular enhancements were found among the masses. Among the 3 patients who underwent MRI, all had lesions with an isointense signal on T1WI. On T2WI, all subcutaneous and infiltrative parotid lesions showed heterogeneous high intensities, whereas lymphadenopathies showed homogeneous high intensities; flow voids were observed in all lesions as hypointense foci. All masses showed a heterogeneously intense enhancement with curvilinear and linear hyposignal intensity.

TABLE 1. Clinical Features of 5 Patients With KD No. 1 2 3 4 5

Age (Years)

Sex

Clinical Presentation

51 21 42 23 54

M M M M M

Painless, slowly growing mass, left retroauricular Painless mass, left retroauricular Painless, slowly growing mass, left parotid region Painless, slowly growing mass around the right ear Painless, slowly growing mass around the left ear, swelling of the right retroauricular region

Duration of Symptoms (Year)

Peripheral Eosinophilia (%)a

Treatment

10 4 3 17 1

NA NA 33.2 NA 17.7

Surgical excision Surgical excision Surgical excision, radiotherapy Surgical excision Radiotherapy

a

Reference range, 1% to 5%; NA, not available.

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Study of DWI and MRSI in Kimura Disease

TABLE 2. Computed Tomographic and MRI Findings of the KD in 5 Patients Imaging Characteristic

No. 1

No. 2

No. 3

Location

Left R

Bilateral R, left parotid region

Left R and parotid region

Single Ill-defined Isodense

Multiple Ill-defined Isodense

Single Ill-defined Isodense

Single Ill-defined —

Homogeneous Moderate

Heterogeneous Moderate

Heterogeneous Moderate



Homogeneous Moderate

— —

Iso- on T1WI Hyper- on T2WI Heterogeneous Intense

Iso- on T1WI Hyper- on T2WI Heterogeneous Intense

Iso- on T1WI Hyper- on T2WI Heterogeneous Intense

——— ———

No

Left IIA, IIB

Left IB, IIB, III, VA Right IIA, IIB

Left VA Right VA

Left IIB Right VA

Number Margin Density on precontrast CT scans Enhancement on postcontrast CT scans Signal intensity on MRI Enhancement on postcontrast MRI Lymphadenopathy

No. 4 Right R and parotid region

No. 5 Left auricular and bilateral R region Multiple Ill-defined Isodense

R, retroauricular; Hypo, hypointense; Iso, isointense; Hyper, hyperintense.

Diffusion-Weighted Imaging On the ADC maps, all subcutaneous and infiltrative parotid lesions had higher ADCs compared with the contralateral normal parotid gland. The mean ADC values of the contralateral normal parotid glands, subcutaneous and infiltrative parotid lesions, as well as lymphadenopathies in patients 2, 3, and 4 are summarized in Table 3.

Multivoxel MR Spectroscopy Spectra acquired from the contralateral normal parotid glands of patients 2, 3, and 4 for comparison showed the presence of lipids but no detectable levels of Cho or Cr. Broad and intense overlapping peaks derived from fatty acids in the chemical shift range of 0.90 to 2.02 ppm were present on all spectra. Lactate doublets (1.32 ppm), which were in the same chemical shift range as fatty acids, were not identifiable on any of the spectra. The metabolic map of the Cho/Cr ratio showed remarkable heterogeneity in patient 2 (Fig 1C). The highest ratio of the area under the resonance peaks of choline (Cho) and creatine (Cr) detected in patients 2, 3, and 4 were shown in Table 3.

frequently associated with KD, with a reported incidence of 42% to 100%.16 Although KD is generally benign and self-limited, it may be complicated by renal involvement, notably nephritic syndrome.15 Whereas the cause of KD remains unknown, it may be a self-limiting allergic or autoimmune response to unknown stimuli. Fine needle aspiration cytology is essential in the basic workup of many tumors of the head and neck.18 However, the cytological features of KD are not specific,19 and the spectrum of cytological features observed in KD may be mimicked by a variety of lesions.20 Confirmation of the diagnosis of KD should be established by histopathology, although the fine needle aspiration cytology may provide some suggestion of KD.19 Histologically, KD is a chronic inflammatory disease characterized by dense collagen fibrosis, capillary proliferation, and chronic inflammation by infiltrating plasma cells, lymphocytes, reactive lymphoid follicles, and eosinophils.2,16,17 Clinically, KD lesions are often misdiagnosed as salivary gland

DISCUSSION Most patients with KD present with firm, painless, single, or multiple subcutaneous lesions in the head and neck, particularly in the parotid and submandibular regions.17 Lymphadenopathy is

TABLE 3. Results of DWI, MRSI, and PWI on KD Patient No. 2

3

4

Site

ADC Values (mm2 s−1)

SIPL LYM NPG SIPL LYM NPG SIPL LYM NPG

1.30 0.69 0.95 1.60 0.72 0.89 1.47 0.59 1.01

−3

 10  10−3  10−3  10−3  10−3  10−3  10−3  10−3  10−3

Highest Cho/Cr 1.20 14.50 ND 1.15 NA ND 1.25 NA ND

SIPL, subcutaneous and infiltrative parotid lesions; LYM, lymphadenopathies; NPG, normal parotid gland; ND, not detected.

FIGURE 1. Patient 2. A, Postcontrast axial CT shows ill-defined subcutaneous masses (arrow) with heterogeneous enhancement and 2 lymph nodes (arrowhead). B, Subcutaneous lesions (arrow) and lymphadenopathies (arrowhead) have high intensities on axial T2WI. C, ADC map shows lymphadenopathy (arrowhead) has lower ADC values compared with subcutaneous lesions (arrow). D, The red voxels within lymphadenopathy have highest detected Cho/Cr levels and the one with Cho/Cr ratio of 12.9 is used for analysis. E, The sum of lymphadenopathy MR spectra. F, Lymphadenopathies have prominent lymphoid follicular hyperplasia with reactive germinal centers (HE, 40).

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FIGURE 2. Kimura disease in patient 3 in the postauricular and left parotid regions. A, Axial contrast-enhanced CT shows an ill-defined mass with a patchy nonenhancement region (arrow) and a large lymph node (red arrowhead) with intense enhancement in the mass. B, Axial T2WI shows an ill-defined mass with hyperintensity. The size of the lymph node (red arrowhead) is 2.9  1.7 cm. The volume of interest (the area outlined in white) of MRSI is superimposed on (B). C, The ADC map shows that the subcutaneous and infiltrative parotid lesions (arrow) have higher ADC values than the normal right parotid gland (white arrowhead), whereas the lymphadenopathy (red arrowhead) has lower ADC values than the normal parotid gland. D, The subcutaneous and infiltrative parotid lesions show relative homogeneity in the Cho/Cr map. E, Photomicrograph of the subcutaneous lesions shows hyperplastic follicles with diffuse eosinophilic infiltration, prominent vasculature, and dense collagen fibrosis (hematoxylin-eosin, original magnification 40).

malignancy because of the diffuse nature of the disease.6,12,13 However, it is imperative to differentiate KD from salivary gland malignancy because of the different treatments and prognoses of the diseases. Although the manifestation of KD in the head and neck region on CT and conventional MRI has been noted in several reports, the findings are nonspecific and variable.3,4,6,12–16 First, on precontrast CT and MRI scans, KD may appear as either welldefined nodular masses or ill-defined plaquelike infiltrative masses in the subcutaneous tissue with or without lymphadenopathy. Second, on conventional MRI, the masses have been reported to show variable signal intensity on both T1WIs and T2WIs. Third, the enhancement patterns vary from mild to intense and from homogeneous to heterogeneous on postcontrast CT and MRI. The variability of signal intensity on MR images and the degree of enhancement on CT and MR images mentioned previously are thought to result from the different degrees of fibrosis and vascular proliferation contained in the individual lesions. Takahashi et al14 reported that prominent fibrotic tissue influenced the intensity on T2WIs, showing less T2 hyperintensity. Abundant vascular proliferation may explain the presence of enhancement and signal intensity–void structures on MR images. However, DWI and MRSI are independent of anatomic information and may be used to characterize lesions that are indefinite on CT and conventional MRI. Additionally, specific and quantitative values can be calculated to significantly improve the accuracy and credibility of the diagnosis of KD. Hence, the inadequacy of CT and conventional MRI can be improved with the application of DWI and MRSI in the diagnosis of KD. In malignant parotid tumors, water molecule diffusion has been shown to be restricted to an abundance of diffusion barriers such as hypercellularity, enlarged and hyperchromatic nuclei, and macromolecular proteins. These restrictions result in low ADC values for malignant tumors compared with benign tumors. Although there are some exceptions, DWI is a potential technique for differentiating benign from malignant salivary gland tumors.

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In our study, the subcutaneous and infiltrative parotid lesions had high ADCs compared with the contralateral normal parotid gland on ADC maps in all 3 patients. The increased ADCs of the lesions may be due to the prominent capillary proliferation and abundant extracellular fluid in the follicular portions. Wang et al7 reported that an ADC value of less than 1.22  10−3 mm2 s−1 was one of the criteria for predicting malignancy in head and neck lesions. As shown in Figure 2 (A, B) for patient 3, KD needs to be distinguished from a malignant tumor based on the findings of diffuse masses on CT and conventional MRI. As the ADC values of our data were higher than the threshold value, malignancy could be excluded. Recently, the usefulness of DWI in the characterization of cervical lymph nodes has been reported. Typically, the ADC values of benign lymph nodes range between 1.2 and 1.4  10−3 mm2 s−1.9 However, the mean ADC values of lymphadenopathies were much lower than those of subcutaneous and infiltrative parotid lesions, which was in accordance with previous relative studies.6,9 Lymphadenopathies of KD were characterized by reactive changes in the lymph nodes that manifested as multiple germinal centers and fibrotic stroma, which could decrease the ADC values. Furthermore, the ADC values of subcutaneous and infiltrative parotid lesions in our study were similar to those of Horikoshi's,6 but the mean ADC values of lymphadenopathies were a bit lower than theirs. It may be because the lymphadenopathies in our study had different degrees of lymphoid follicular hyperplasia, eosinophilic infiltration, microvascular proliferation, and so on from theirs. Hence, the low ADC values of lymphadenopathies combined with the high ADC values of subcutaneous and infiltrative parotid lesions may be characteristic of KD. Furthermore, KD must be differentiated from malignant lymphoma with lymph node and soft tissue lesions in particular, and this has been reported having a low mean ADC value of 0.66 ± 0.17  10−3 mm2 s−1. 7 However, King et al21 observed that non-Hodgkin lymphoma (NHL) showed intermediate signal intensity on T2WIs and had mild or moderate enhancement after contrast administration. In our study, all subcutaneous and infiltrative parotid KD lesions showed heterogeneous high intensities on T2WIs and had high ADC values, whereas lymphadenopathies showed homogeneous high intensities on T2WIs. We therefore speculated that the differentiation of KD from malignant lymphoma may be aided by the high ADC values, heterogeneous high intensities on T2WIs, and intense enhancement of subcutaneous and infiltrative parotid lesions combined with the homogenous high intensity on T2WIs and intense enhancement of lymphadenopathies observed in KD. An elevated Cho level, which is a marker of membrane turnover, is found not only in malignant tumors but also in benign tumors that are hypercellular and in areas with active inflammation.10 In our study, the Cho/Cr ratios of subcutaneous and infiltrative parotid lesions in all 3 patients were slightly increased and were dramatically smaller than that of lymphadenopathy in patient 2. The increased Cho/Cr values of infiltrative parotid lesions in all 3 patients were most likely due to increased cellularity. Additionally, because hypercellularity was more prominent in reactive lymphadenopathies than subcutaneous and infiltrative parotid lesions, the areas with a high Cho/Cr ratio in patient 2 were intraparotid lymphadenopathies. Although we only detected the Cho/Cr ratio in one node of patient 2 and the Cr concentration was low in the lesions or difficult to be measured, these phenomena were consistent with previous study,10 which need to be validated by more cases. The significantly high Cho/Cr ratio (14.5) of the KD lymphadenopathies was largely due to the large number of inflammatory cells, which was consistent with the study of King et al.11 They observed the highest Cho/Cr ratio (15.5) for cervical lymphadenopathies in Castleman disease, followed by NHL (9.1) and undifferentiated carcinoma (4.4), among others.11 In our study, the Cho/Cr ratio of lymphadenopathy in KD was similar to that of another type of © 2014 Mutaz B. Habal, MD

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The Journal of Craniofacial Surgery • Volume 25, Number 6, November 2014

lymphoproliferative disorder of Castleman disease.11,22 In addition, Bisdas et al23 also reported a mean Cho/Cr ratio of 5.7 in NHL of the sphenoid sinus, which was lower than that of lymphadenopathy in KD observed in our study. Therefore, the relatively low Cho/Cr ratios of subcutaneous and infiltrative parotid lesions and the high Cho/Cr ratios of lymphadenopathies may be characteristics of KD, which can suggest the diagnosis of KD. The main limitation of this study was that we included only a small number of patients. Moreover, high-field magnets and improved radiofrequency coils should be used in the future, resulting in better signal detection, to allow further reduction of the voxel size and an improvement of spatial resolution. In conclusion, subcutaneous and infiltrative parotid lesions with dramatically increased ADC values associated with low ADC values for lymphadenopathies on DWI are important characteristics of KD. In addition, the obviously increased Cho/Cr ratio of lymphadenopathies on MRSI can further suggest the diagnosis of KD. The DWI and MRSI features of KD combined with the findings of CT and conventional MRI can highly suggest the diagnosis of KD. ACKNOWLEDGMENTS This work was supported by the Crossover Study Fund of Basic & Clinical Medicine of Shanghai Medical School of Fudan University (Z-259).

REFERENCES 1. Chen H, Thompson LD, Aguilera NS, et al. Kimura disease: a clinicopathologic study of 21 cases. Am J Surg Pathol 2004;28:505–513 2. Li TJ, Chen XM, Wang SZ, et al. Kimura's disease: a clinicopathologic study of 54 Chinese patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82:549–555 3. Park JS, Jin W, Ryu KN, et al. Bilateral asymmetric superficial soft tissue masses with extensive involvement of both upper extremities: demonstration of Kimura's disease by US and MRI (2008: 12b). Eur Radiol 2009;19:781–786 4. Jeong YY, Song SK, Heo SH, et al. Imaging of Kimura's disease involving the abdomen. AJR Am J Roentgenol 2006;187:W131–W132 5. Eida S, Sumi M, Sakihama N, et al. Apparent diffusion coefficient mapping of salivary gland tumors: prediction of the benignancy and malignancy. AJNR Am J Neuroradiol 2007;28:116–121

Study of DWI and MRSI in Kimura Disease

6. Horikoshi T, Motoori K, Ueda T, et al. Head and neck MRI of Kimura disease. Br J Radiol 2011;84:800–804 7. Wang J, Takashima S, Takayama F, et al. Head and neck lesions: characterization with diffusion-weighted echo-planar MR imaging. Radiology 2001;220:621–630 8. Holzapfel K, Duetsch S, Fauser C, et al. Value of diffusion-weighted MR imaging in the differentiation between benign and malignant cervical lymph nodes. Eur J Radiol 2009;72:381–387 9. Muenzel D, Duetsch S, Fauser C, et al. Diffusion-weighted magnetic resonance imaging in cervical lymphadenopathy: report of three cases of patients with Bartonella henselae infection mimicking malignant disease. Acta Radiol 2009;50:914–916 10. King AD, Yeung DK, Ahuja AT, et al. Salivary gland tumors at in vivo proton MR spectroscopy. Radiology 2005;237:563–569 11. King AD, Yeung DK, Ahuja AT, et al. Human cervical lymphadenopathy: evaluation with in vivo 1H-MRS at 1.5 T. Clin Radiol 2005;60:592–598 12. Zhang R, Ban XH, Mo YX, et al. Kimura's disease: the CT and MRI characteristics in fifteen cases. Eur J Radiol 2011;80:489–497 13. Park SW, Kim HJ, Sung KJ, et al. Kimura disease: CT and MR imaging findings. AJNR Am J Neuroradiol 2012;33:784–788 14. Takahashi S, Ueda J, Furukawa T, et al. Kimura disease: CT and MR findings. AJNR Am J Neuroradiol 1996;17:382–385 15. Goldenberg D, Gatot A, Barki Y, et al. Computerized tomographic and ultrasonographic features of Kimura's disease. J Laryngol Otol 1997;111:389–391 16. Gopinathan A, Tan TY. Kimura's disease: imaging patterns on computed tomography. Clin Radiol 2009;64:994–999 17. Oguz KK, Ozturk A, Cila A. Magnetic resonance imaging findings in Kimura's disease. Neuroradiology 2004;46:855–858 18. Lin AC, Bhattacharyya N. The utility of fine needle aspiration in parotid malignancy. Otolaryngol Head Neck Surg 2007;136:793–798 19. Viswanatha B. Kimura's disease in children: a 9 years prospective study. Int J Pediatr Otorhinolaryngol 2007;71:1521–1525 20. Deshpande AH, Nayak S, Munshi MM, et al. Kimura's disease. Diagnosis by aspiration cytology. Acta Cytol 2002;46:357–363 21. King AD, Lei KI, Richards PS, et al. Non-Hodgkin's lymphoma of the nasopharynx: CT and MR imaging. Clin Radiol 2003;58:621–625 22. Talat N, Belgaumkar AP, Schulte KM. Surgery in Castleman's disease: a systematic review of 404 published cases. Ann Surg 2012;255:677–684 23. Bisdas S, Fetscher S, Feller AC, et al. Primary B cell lymphoma of the sphenoid sinus: CT and MRI characteristics with correlation to perfusion and spectroscopic imaging features. Eur Arch Otorhinolaryngol 2007;264:1207–1213

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Preliminary study of diffusion-weighted imaging and magnetic resonance spectroscopy imaging in Kimura disease.

In this study, we evaluated the value of diffusion-weighted imaging (DWI) and magnetic resonance (MR) spectroscopy imaging (MRSI) combined with comput...
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