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Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
bidity for certain tumor subtypes [9,10]. Rarely, en bloc resection for metastatic spine tumors can be considered when long term survival is expected (given reasonable risks with surgery) [11–14]. Furthermore, although chemotherapy and/or radiotherapy have shown modest benefit in a few cases of metastatic EMC to other sites [8], interval progression despite adjuvant radiotherapy provided a rationale for surgical intervention. 4. Conclusion EMC is a rare salivary gland tumor that should be considered in the differential diagnosis for spinal lesions, in patients who have a prior history of a parotid gland tumor or an unclassified head and neck neoplasm. GTR with or without wide tumor free margins may be considered for patients diagnosed with EMC metastasized to the spinal column. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Corio RL, Sciubba JJ, Brannon RB, et al. Epithelial-myoepithelial carcinoma of intercalated duct origin. A clinicopathologic and ultrastructural assessment of sixteen cases. Oral Surg Oral Med Oral Pathol 1982;53:280–7.
[2] Donath K, Seifert G, Schmitz R. [Diagnosis and ultrastructure of the tubular carcinoma of salivary gland ducts. Epithelial-myoepithelial carcinoma of the intercalated ducts]. Virchows Arch A Pathol Pathol Anat 1972;356:16–31. [3] Friedrich RE, Donath K. Epithelial-myoepithelial carcinoma of the parotid gland with multiple distant metastases: a case report. J Oral Maxillofacial Surg 2000;58:690–4. [4] Morinaga S, Hashimoto S, Tezuka F. Epithelial-myoepithelial carcinoma of the parotid gland in a child. Acta Pathol Jpn 1992;42:358–63. [5] Noel S, Brozna JP. Epithelial-myoepithelial carcinoma of salivary gland with metastasis to lung: report of a case and review of the literature. Head Neck 1992;14:401–6. [6] Seethala RR. Oncocytic and apocrine epithelial myoepithelial carcinoma: novel variants of a challenging tumor. Head Neck Pathol 2013;7:S77–84. [7] Soomro IN, Hussainy AS, Chishti K, et al. Spinal cord compression caused by metastatic epithelial myoepithelial carcinoma of the parotid gland. J Pak Med Assoc 1999;49:249–50. [8] Yamazaki H, Ota Y, Aoki T, et al. Lung metastases of epithelial-myoepithelial carcinoma of the parotid gland successfully treated with chemotherapy: a case report. J Oral Maxillofacial Surg 2013;71:220–6. [9] Kaloostian PE, Zadnik PL, Etame AB, et al. Surgical management of primary and metastatic spinal tumors. Cancer Control 2014;21:133–9. [10] Katonis P, Alpantaki K, Michail K, et al. Spinal chondrosarcoma: a review. Sarcoma 2011;2011:378957. [11] Kaloostian PE, Zadnik PL, Awad AJ, et al. En bloc resection of a pheochromocytoma metastatic to the spine for local tumor control and for treatment of chronic catecholamine release and related hypertension. J Neurosurg 2013;18:611–6. [12] Sciubba DM, Petteys RJ, Shakur SF, et al. En bloc spondylectomy for treatment of tumor-induced osteomalacia. J Neurosurg 2009;11:600–4. [13] Sundaresan N, Boriani S, Rothman A, et al. Tumors of the osseous spine. J Neurooncol 2004;69:273–90. [14] Yao KC, Boriani S, Gokaslan ZL, et al. En bloc spondylectomy for spinal metastases: a review of techniques. Neurosurg Focus 2003;15:E6.
http://dx.doi.org/10.1016/j.jocn.2015.07.013
Demyelination preceding a diagnosis of central nervous system lymphoma Sarah Kalus a,⇑, Bruno Di Muzio a, Frank Gaillard a,b a b
Department of Radiology, 1st Floor, 1B Building, The Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia Department of Radiology, The University of Melbourne, Parkville, Australia
a r t i c l e
i n f o
Article history: Received 20 July 2015 Accepted 24 July 2015
Keywords: Multiple sclerosis Neuroradiology Primary central nervous system lymphoma Tumefactive demyelination
a b s t r a c t We present a case of primary central nervous system lymphoma (PCNSL) co-existing with demyelination in a young immunocompetent woman. The patient presented with an expansile, enhancing lesion in the right occipital lobe which was initially attributed to tumefactive demyelination and subsequently proven to be PCNSL. PCNSL is an uncommon malignancy, particularly in young immunocompetent patients, and on MRI classically manifests as a homogeneously enhancing solitary mass with a predilection for periventricular and superficial locations, often contacting ventricular and meningeal surfaces. Tumefactive demyelinating lesions typically present as large white matter lesions with little mass effect or vasogenic oedema and ‘‘open-ring” enhancement, with the incomplete portion of the ring on the grey matter side of the lesion. PCNSL and tumefactive demyelinating lesions share some radiological features and thus, as our case report highlights, differentiating between them can be challenging. We discuss how the application of conventional and advanced MRI techniques combined with clinical and laboratory findings can lead to a precise diagnosis, potentially obviating the need for biopsy and facilitating prompt and appropriate treatment. Ó 2015 Elsevier Ltd. All rights reserved.
1. Case report A 26-year-old previously well, immunocompetent woman presented with a 3 month history of headaches and visual blurring. Cerebrospinal fluid analysis revealed features of chronic ⇑ Corresponding author. Tel.: +61 3 9342 7255; fax: +61 3 9342 8602. E-mail address: [email protected] (S. Kalus).
inflammation with no evidence of malignancy. MRI demonstrated multiple bilateral periventricular T2 and fluid attenuated inversion recovery (FLAIR) hyperintense lesions (Fig. 1F) of which several enhanced. In addition, there was a moderate-sized region of cortical expansion in the right occipital lobe which displayed high T2 and FLAIR signal with vivid enhancement and diffusion restriction (Fig. 1A–E). Magnetic resonance spectroscopy (MRS) demonstrated elevated choline:creatine and lactate and glutamine/glutamate
Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
peaks in the right occipital lesion. The appearances were favoured to represent demyelination, specifically acute disseminated encephalomyelitis or Marburg’s variant of multiple sclerosis (MS). The nature of the right occipital lesion was unclear; possibilities raised included tumefactive demyelination and subacute infarct. The patient underwent biopsy of a left frontal lesion, selected as least likely to result in morbidity. Histology revealed demyelination and prominent perivascular cuffs of lymphoid cells comprising polyclonal CD3+ T and CD20+ B lymphocytes, suggesting inflammatory demyelination with no evidence of malignancy. The patient was treated with prednisolone and natalizumab. The headaches improved and appearances on two follow-up MRI studies were stable. She returned 4 months after the initial presentation, however, with worsened headaches and confusion. MRI showed progression of periventricular FLAIR hyperintensity (Fig. 2F). The right occipital lesion demonstrated marked expansion with mass effect, far more intense gyriform enhancement and persistent diffusion restriction (Fig. 2A–E). It was concluded that the evolution of the right occipital lesion was difficult to reconcile with demyelination or infarct and that central nervous system lymphoma was the most likely diagnosis. Biopsy of the right occipital lesion confirmed a diagnosis of non-Hodgkin diffuse large B cell lymphoma. Chemotherapy was commenced and clinical and imaging improvement ensued, with no evidence of lymphoma on the most recent MRI 12 months following initial presentation. 2. Discussion Primary central nervous system lymphoma (PCNSL) is an uncommon malignancy accounting for 1–5% of intracranial neoplasms, typically presenting sporadically in the fifth and sixth decades of life with a female predominance [1]. They are usually diffuse large B cell non-Hodgkin lymphomas and have a poor prognosis, with a median survival of 2–3 months when untreated. In immunocompetent patients, PCNSL classically manifests as a
147
homogeneously enhancing solitary mass with a predilection for periventricular and superficial locations, often contacting ventricular and meningeal surfaces [1]. Tumefactive demyelinating lesions (TDL), in contrast, are large (greater than 2 cm) lesions mimicking tumour and often lead to biopsy [2]. TDL typically present as large white matter lesions with little mass effect or vasogenic oedema and ‘‘open-ring” enhancement, with the incomplete portion of the ring on the grey matter side of the lesion. Eighty-five percent of patients with TDL have additional white matter lesions [2]. PCNSL and TDL thus share some radiological features and differentiating between them can be challenging, particularly when unusual imaging or clinical manifestations are encountered. Complicating the discussion is that in rare instances like this case, both MS and PCNSL may occur in the same patient. After commencing corticosteroids, TDL may take over 12 weeks to show significant imaging improvement, and enhancement persists in 2% of demyelinating lesions after 6 months [2]. PCNSL can also show considerable radiological and clinical improvement with corticosteroids, however relapse inevitably occurs typically within 6–12 months [2]. Imaging can aid in discriminating between PCNSL and TDL. Features that favour TDL include open-ring enhancement, mixed iso- and hyper-intense T2 signal of enhancing components, and lack of cortical involvement and mass effect [3]. PCNSL, on the other hand, exhibits hypo- or iso-intense T2 signal and more marked perilesional oedema [4]. Furthermore, CT hypoattenuation of MRI enhancing regions is highly specific for distinguishing TDL from PCNSL, and MRI in combination with non-contrast CT is significantly more accurate than MRI alone [3]. PCNSL characteristically demonstrates intense diffusion restriction whilst TDL frequently display elevated apparent diffusion coefficient (ADC). Although acute demyelinating lesions may have peripheral diffusion restriction corresponding to the region of open-ring enhancement, the ADC in TDL is not as low as in PCNSL [5]. The role of MRS in discriminating between these entities is not yet established. In PCNSL, MRS reveals a non-specific tumour
Fig. 1. Axial MRI of right occipital lesion displaying low T1 signal (A), contrast enhancement (B) and high T2 signal (C). High signal on diffusion weighted imaging (D) represents restricted diffusion on the apparent diffusion coefficient map (E). Periventricular T2 hyperintensities were also seen (F).
148
Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
Fig. 2. Axial MRI of right occipital lesion demonstrating progression 4 months following initial presentation with low T1 signal (A), contrast enhancement (B) and high T2 and fluid attenuated inversion recovery signal (C and F). High signal on diffusion weighted imaging (D) represents restricted diffusion on the apparent diffusion coefficient map (E).
pattern of increased lipid, choline:creatine and myo-inositol and decreased N-acetylaspartate [1]. This pattern is also observed in the acute phase of TDL, although elevated glutamate/glutamine peaks favour TDL [6]. Moreover, serial MRS may be more contributory than a single study as spectroscopy classically changes as TDL age whilst remaining stable in neoplasms [2]. Finally, relative cerebral blood volume is significantly lower in TDL than in PCNSL [4].
3. Conclusion In a patient with a known diagnosis of MS presenting with a mass-like lesion not characteristic of tumefactive demyelination, alternative diagnoses should be sought. Distinguishing between PCNSL and TDL can be challenging. Using conventional and advanced MRI techniques combined with clinical and laboratory findings, however, PCNSL and TDL can be differentiated with confidence, potentially obviating the need for biopsy and facilitating prompt and appropriate treatment. http://dx.doi.org/10.1016/j.jocn.2015.07.013
4. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Haldorsen IS, Espeland A, Larsson E-M. Central nervous system lymphoma: characteristic findings on traditional and advanced imaging. AJNR Am J Neuroradiol 2011;32:984–92. [2] Hardy TA, Chataway J. Tumefactive demyelination: an approach to diagnosis and management. J Neurol Neurosurg Psychiatry 2013;84:1047–53. [3] Kim DS, Na DG, Kim KH, et al. Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging. Radiology 2009;251:467–75. [4] Cha S, Pierce S, Knopp EA, et al. Dynamic contrast-enhanced T2⁄-weighted MR imaging of tumefactive demyelinating lesions. AJNR Am J Neuroradiol 2001;22: 1109–16. [5] Lu SS, Kim SJ, Kim N, et al. Histogram analysis of apparent diffusion coefficient maps for differentiating primary CNS lymphomas from tumefactive demyelinating lesions. AJR Am J Roentgenol 2015;204:827–34. [6] Husseini L, Saleh A, Reifenberger G, et al. Inflammatory demyelinating brain lesions heralding primary CNS lymphoma. Can J Neurol Sci 2012;39:6–10.
Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
bidity for certain tumor subtypes [9,10]. Rarely, en bloc resection for metastatic spine tumors can be considered when long term survival is expected (given reasonable risks with surgery) [11–14]. Furthermore, although chemotherapy and/or radiotherapy have shown modest benefit in a few cases of metastatic EMC to other sites [8], interval progression despite adjuvant radiotherapy provided a rationale for surgical intervention. 4. Conclusion EMC is a rare salivary gland tumor that should be considered in the differential diagnosis for spinal lesions, in patients who have a prior history of a parotid gland tumor or an unclassified head and neck neoplasm. GTR with or without wide tumor free margins may be considered for patients diagnosed with EMC metastasized to the spinal column. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Corio RL, Sciubba JJ, Brannon RB, et al. Epithelial-myoepithelial carcinoma of intercalated duct origin. A clinicopathologic and ultrastructural assessment of sixteen cases. Oral Surg Oral Med Oral Pathol 1982;53:280–7.
[2] Donath K, Seifert G, Schmitz R. [Diagnosis and ultrastructure of the tubular carcinoma of salivary gland ducts. Epithelial-myoepithelial carcinoma of the intercalated ducts]. Virchows Arch A Pathol Pathol Anat 1972;356:16–31. [3] Friedrich RE, Donath K. Epithelial-myoepithelial carcinoma of the parotid gland with multiple distant metastases: a case report. J Oral Maxillofacial Surg 2000;58:690–4. [4] Morinaga S, Hashimoto S, Tezuka F. Epithelial-myoepithelial carcinoma of the parotid gland in a child. Acta Pathol Jpn 1992;42:358–63. [5] Noel S, Brozna JP. Epithelial-myoepithelial carcinoma of salivary gland with metastasis to lung: report of a case and review of the literature. Head Neck 1992;14:401–6. [6] Seethala RR. Oncocytic and apocrine epithelial myoepithelial carcinoma: novel variants of a challenging tumor. Head Neck Pathol 2013;7:S77–84. [7] Soomro IN, Hussainy AS, Chishti K, et al. Spinal cord compression caused by metastatic epithelial myoepithelial carcinoma of the parotid gland. J Pak Med Assoc 1999;49:249–50. [8] Yamazaki H, Ota Y, Aoki T, et al. Lung metastases of epithelial-myoepithelial carcinoma of the parotid gland successfully treated with chemotherapy: a case report. J Oral Maxillofacial Surg 2013;71:220–6. [9] Kaloostian PE, Zadnik PL, Etame AB, et al. Surgical management of primary and metastatic spinal tumors. Cancer Control 2014;21:133–9. [10] Katonis P, Alpantaki K, Michail K, et al. Spinal chondrosarcoma: a review. Sarcoma 2011;2011:378957. [11] Kaloostian PE, Zadnik PL, Awad AJ, et al. En bloc resection of a pheochromocytoma metastatic to the spine for local tumor control and for treatment of chronic catecholamine release and related hypertension. J Neurosurg 2013;18:611–6. [12] Sciubba DM, Petteys RJ, Shakur SF, et al. En bloc spondylectomy for treatment of tumor-induced osteomalacia. J Neurosurg 2009;11:600–4. [13] Sundaresan N, Boriani S, Rothman A, et al. Tumors of the osseous spine. J Neurooncol 2004;69:273–90. [14] Yao KC, Boriani S, Gokaslan ZL, et al. En bloc spondylectomy for spinal metastases: a review of techniques. Neurosurg Focus 2003;15:E6.
http://dx.doi.org/10.1016/j.jocn.2015.07.013
Demyelination preceding a diagnosis of central nervous system lymphoma Sarah Kalus a,⇑, Bruno Di Muzio a, Frank Gaillard a,b a b
Department of Radiology, 1st Floor, 1B Building, The Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia Department of Radiology, The University of Melbourne, Parkville, Australia
a r t i c l e
i n f o
Article history: Received 20 July 2015 Accepted 24 July 2015
Keywords: Multiple sclerosis Neuroradiology Primary central nervous system lymphoma Tumefactive demyelination
a b s t r a c t We present a case of primary central nervous system lymphoma (PCNSL) co-existing with demyelination in a young immunocompetent woman. The patient presented with an expansile, enhancing lesion in the right occipital lobe which was initially attributed to tumefactive demyelination and subsequently proven to be PCNSL. PCNSL is an uncommon malignancy, particularly in young immunocompetent patients, and on MRI classically manifests as a homogeneously enhancing solitary mass with a predilection for periventricular and superficial locations, often contacting ventricular and meningeal surfaces. Tumefactive demyelinating lesions typically present as large white matter lesions with little mass effect or vasogenic oedema and ‘‘open-ring” enhancement, with the incomplete portion of the ring on the grey matter side of the lesion. PCNSL and tumefactive demyelinating lesions share some radiological features and thus, as our case report highlights, differentiating between them can be challenging. We discuss how the application of conventional and advanced MRI techniques combined with clinical and laboratory findings can lead to a precise diagnosis, potentially obviating the need for biopsy and facilitating prompt and appropriate treatment. Ó 2015 Elsevier Ltd. All rights reserved.
1. Case report A 26-year-old previously well, immunocompetent woman presented with a 3 month history of headaches and visual blurring. Cerebrospinal fluid analysis revealed features of chronic ⇑ Corresponding author. Tel.: +61 3 9342 7255; fax: +61 3 9342 8602. E-mail address: [email protected] (S. Kalus).
inflammation with no evidence of malignancy. MRI demonstrated multiple bilateral periventricular T2 and fluid attenuated inversion recovery (FLAIR) hyperintense lesions (Fig. 1F) of which several enhanced. In addition, there was a moderate-sized region of cortical expansion in the right occipital lobe which displayed high T2 and FLAIR signal with vivid enhancement and diffusion restriction (Fig. 1A–E). Magnetic resonance spectroscopy (MRS) demonstrated elevated choline:creatine and lactate and glutamine/glutamate
Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
peaks in the right occipital lesion. The appearances were favoured to represent demyelination, specifically acute disseminated encephalomyelitis or Marburg’s variant of multiple sclerosis (MS). The nature of the right occipital lesion was unclear; possibilities raised included tumefactive demyelination and subacute infarct. The patient underwent biopsy of a left frontal lesion, selected as least likely to result in morbidity. Histology revealed demyelination and prominent perivascular cuffs of lymphoid cells comprising polyclonal CD3+ T and CD20+ B lymphocytes, suggesting inflammatory demyelination with no evidence of malignancy. The patient was treated with prednisolone and natalizumab. The headaches improved and appearances on two follow-up MRI studies were stable. She returned 4 months after the initial presentation, however, with worsened headaches and confusion. MRI showed progression of periventricular FLAIR hyperintensity (Fig. 2F). The right occipital lesion demonstrated marked expansion with mass effect, far more intense gyriform enhancement and persistent diffusion restriction (Fig. 2A–E). It was concluded that the evolution of the right occipital lesion was difficult to reconcile with demyelination or infarct and that central nervous system lymphoma was the most likely diagnosis. Biopsy of the right occipital lesion confirmed a diagnosis of non-Hodgkin diffuse large B cell lymphoma. Chemotherapy was commenced and clinical and imaging improvement ensued, with no evidence of lymphoma on the most recent MRI 12 months following initial presentation. 2. Discussion Primary central nervous system lymphoma (PCNSL) is an uncommon malignancy accounting for 1–5% of intracranial neoplasms, typically presenting sporadically in the fifth and sixth decades of life with a female predominance [1]. They are usually diffuse large B cell non-Hodgkin lymphomas and have a poor prognosis, with a median survival of 2–3 months when untreated. In immunocompetent patients, PCNSL classically manifests as a
147
homogeneously enhancing solitary mass with a predilection for periventricular and superficial locations, often contacting ventricular and meningeal surfaces [1]. Tumefactive demyelinating lesions (TDL), in contrast, are large (greater than 2 cm) lesions mimicking tumour and often lead to biopsy [2]. TDL typically present as large white matter lesions with little mass effect or vasogenic oedema and ‘‘open-ring” enhancement, with the incomplete portion of the ring on the grey matter side of the lesion. Eighty-five percent of patients with TDL have additional white matter lesions [2]. PCNSL and TDL thus share some radiological features and differentiating between them can be challenging, particularly when unusual imaging or clinical manifestations are encountered. Complicating the discussion is that in rare instances like this case, both MS and PCNSL may occur in the same patient. After commencing corticosteroids, TDL may take over 12 weeks to show significant imaging improvement, and enhancement persists in 2% of demyelinating lesions after 6 months [2]. PCNSL can also show considerable radiological and clinical improvement with corticosteroids, however relapse inevitably occurs typically within 6–12 months [2]. Imaging can aid in discriminating between PCNSL and TDL. Features that favour TDL include open-ring enhancement, mixed iso- and hyper-intense T2 signal of enhancing components, and lack of cortical involvement and mass effect [3]. PCNSL, on the other hand, exhibits hypo- or iso-intense T2 signal and more marked perilesional oedema [4]. Furthermore, CT hypoattenuation of MRI enhancing regions is highly specific for distinguishing TDL from PCNSL, and MRI in combination with non-contrast CT is significantly more accurate than MRI alone [3]. PCNSL characteristically demonstrates intense diffusion restriction whilst TDL frequently display elevated apparent diffusion coefficient (ADC). Although acute demyelinating lesions may have peripheral diffusion restriction corresponding to the region of open-ring enhancement, the ADC in TDL is not as low as in PCNSL [5]. The role of MRS in discriminating between these entities is not yet established. In PCNSL, MRS reveals a non-specific tumour
Fig. 1. Axial MRI of right occipital lesion displaying low T1 signal (A), contrast enhancement (B) and high T2 signal (C). High signal on diffusion weighted imaging (D) represents restricted diffusion on the apparent diffusion coefficient map (E). Periventricular T2 hyperintensities were also seen (F).
148
Case Reports / Journal of Clinical Neuroscience 24 (2016) 146–148
Fig. 2. Axial MRI of right occipital lesion demonstrating progression 4 months following initial presentation with low T1 signal (A), contrast enhancement (B) and high T2 and fluid attenuated inversion recovery signal (C and F). High signal on diffusion weighted imaging (D) represents restricted diffusion on the apparent diffusion coefficient map (E).
pattern of increased lipid, choline:creatine and myo-inositol and decreased N-acetylaspartate [1]. This pattern is also observed in the acute phase of TDL, although elevated glutamate/glutamine peaks favour TDL [6]. Moreover, serial MRS may be more contributory than a single study as spectroscopy classically changes as TDL age whilst remaining stable in neoplasms [2]. Finally, relative cerebral blood volume is significantly lower in TDL than in PCNSL [4].
3. Conclusion In a patient with a known diagnosis of MS presenting with a mass-like lesion not characteristic of tumefactive demyelination, alternative diagnoses should be sought. Distinguishing between PCNSL and TDL can be challenging. Using conventional and advanced MRI techniques combined with clinical and laboratory findings, however, PCNSL and TDL can be differentiated with confidence, potentially obviating the need for biopsy and facilitating prompt and appropriate treatment. http://dx.doi.org/10.1016/j.jocn.2015.07.013
4. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Haldorsen IS, Espeland A, Larsson E-M. Central nervous system lymphoma: characteristic findings on traditional and advanced imaging. AJNR Am J Neuroradiol 2011;32:984–92. [2] Hardy TA, Chataway J. Tumefactive demyelination: an approach to diagnosis and management. J Neurol Neurosurg Psychiatry 2013;84:1047–53. [3] Kim DS, Na DG, Kim KH, et al. Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging. Radiology 2009;251:467–75. [4] Cha S, Pierce S, Knopp EA, et al. Dynamic contrast-enhanced T2⁄-weighted MR imaging of tumefactive demyelinating lesions. AJNR Am J Neuroradiol 2001;22: 1109–16. [5] Lu SS, Kim SJ, Kim N, et al. Histogram analysis of apparent diffusion coefficient maps for differentiating primary CNS lymphomas from tumefactive demyelinating lesions. AJR Am J Roentgenol 2015;204:827–34. [6] Husseini L, Saleh A, Reifenberger G, et al. Inflammatory demyelinating brain lesions heralding primary CNS lymphoma. Can J Neurol Sci 2012;39:6–10.
