Magnetic Resonance Imaging Features of Solitary Inflam m atory Brain Masses Rohit Bakshi, MD Dent Neurologic Institute Millard Fillmore Health System Department of Neurology University of Buffalo State University of New York School of Medicine and Biomedical Sciences Buffalo, NY Jon G lass, MD Department of Neurology New York University School of Medicine New York, NY ABSTRACT Brain lesions in inflammatory diseases may present as solitary masses, prompting a biopsy. We present neuroimaging and his­ tologic findings in five patients with solitary, inflammatory, demyelinating mass lesions located in the supratentorial white matter and gray-white junction. The patients presented with seizures, focal neurologic signs, and neuroimaging findings that indicated the possibility of a neoplasm. Computed tomography (CT) revealed enhancing, single hypodense lesions associated with mild or no mass effect. On MRI, the lesions were hypointense on T1-weighted images and hyperintense on T2weighted images. Variable patterns of enhancement were noted David N. Louis, MD Department of Pathology/ Neuropathology and Neurosurgical Service Massachusetts General Hospita and Harvard Medical School Boston, MA Fred H. Hochberg, MD Department of Neurology Massachusetts General Hospital and Harvard Medical School Boston, MA The finding of an enhancing brain mass lesion on com puted tomography (CT) or magnetic resonance imaging (MRI) studies often prompts a histologic diagnosis^ Although biopsy may lead to a diagnosis of neoplasia, non-neoplastic lesions also are found. Inflammatory, del myelinating lesions rarely are indistinguishable from neo­ plasms on neuroimaging studies.1-16 We present MRI, Cl and pathologic findings in five patients harboring solitary! inflammatory, demyelinating lesions of the supratentorial white matter and gray-white junction, in whom the initial clinical and neuroimaging findings were consistent with a neoplasm, on CT and MRI, including homogeneous/patchy (n = 3) and ring/nodular (n = 1) enhancement. There was no evidence of calcification or hemorrhage. Biopsies revealed a leukoencephali­ tis and demyelination, with varying degrees of demyelination among the cases. The syndrome, relating to a solitary lesion, was corticosteroid-sensitive, and it ultimately stabilized. Exten­ sive longitudinal evaluations failed to reveal multiple sclerosis, infection, or neoplasm. Solitary inflammatory lesions add to the differential diagnosis of large, supratentorial, solitary spaceoccupying lesions noted on CT and MRI scans. Bakshi R, Glass J, Louis DN, Hochberg FH. Magnetic resonance imaging features of solitary inflammatory brain masses. J Neuroimag 1998;8:8-14 M aterials and M ethods Computed tomography and MRI scans were reviewed (RB) and surgical specimens were examined (DNL) of five patients initially seen at Massachusetts General Hos­ F pital from 1977 to 1989. Magnetic resonance imaging stud­ JL ir ies, at 1.0 T or 1.5 T, included conventional spin echo v Tl-weighted images (Tl-W I) and T2-weighted images! (T2-WI). Histologic stains included H and E, Luxol fast] blue, Bodian silver impregnation, and glial fibrillary acid F protein. n 1; Re s u |ts ( Case Reports Received Oct 28, 1996, and in revised form Dec 23, 1996. Ac­ cepted for publication Dec 26, 1996. Address correspondence to Dr Bakshi, Lucy Dent Imaging Center, Millard Fillmore Health System, 3 Gates Circle, Buf­ falo, NY 14209. 8 Patient 1: A 19-year-old woman developed generalized c seizures and a mild left hemiparesis. Computed tomogra- r phy revealed a hypodense mass in the right frontal sub- r cortical white matter, extending to the corpus callosum ( (Table 1). On MRI, the lesion was hypointense on Tl-WI, a hyperintense on T2-WI (Figs 1A, 2A), and showed patchy, r intense enhancement (Fig 2B). Cerebrospinal fluid (CSF) r findings are presented in Table 2. A brain biopsy revealed i demyelination of white matter with axonal preservation, 2 C o pyright © 1998 by th e A m erican Society o f N eu ro im ag in g ) of Fig 1. Patient 1. Serial axial MRI (T2-WI); hyperintense lesion. (A) 4/86 (onset): Right frontal periventricular white matter and gray-white los- junction lesion. (B) 7/86: Reduction in lesion size after corticosteroid therapy. (C) 2/87: Increase in lesion size. (D) 11/87: Further increase :ud- in lesion size. (E) 5/90: Reduction in lesion size after corticosteroid therapy. (F) 4/93: Atrophic lesion with ex-vacuo dilatation of the lateral cho ventricle. iges fast acid perivascular lymphocytes, scattered microglia, parenchy­ cal status and neuroimaging studies remained stable mal macrophages and reactive astrocytes. Three months during the next 3 years. later, corticosteroid therapy led to lesion size reduction (Fig IB). Nineteen months after presentation, the mass Patien t 2: A 66-year-old woman developed left hemipa­ progressively expanded (Figs 1C, D; 2C). Repeat biopsy resis, headaches, and ataxia 6 months after an illness char­ revealed similar changes, including moderate numbers of acterized by adenopathy, fatigue, and an elevated Epsteinchronic inflammatory cells, diffuse, incomplete demyeli- Barr virus viral capsid antigen antibody titer (1:5120). zed nation with axonal and oligodendroglial preservation, and Computed tomography (not shown) revealed a diffusely gra;ub- myelin-laden macrophages. Management with prednisone enhancing right frontal periventricular white matter lesion mm (80 mg/day) led to lesion size reduction (Fig IE) without associated with mild mass effect (Table 1). On MRI (not WI, a change in seizures and hemiparesis. An open biopsy shown), the lesion spared the cortex; it was hypointense on :hy, revealed similar changes. The lesion regressed during the Tl-W I, hyperintense on T2-WI, and irregularly enhancing SF) next 6 years, becoming atrophic (Fig IF), and nonenhanc­ (not shown). Cerebrospinal fluid findings are presented in lied ing (not shown). A frontal lobectomy (performed for sei­ Table 2. An open biopsy revealed perivascular lympho­ ion, zure control) revealed similar findings. The patient’s clini­ cytes, reactive astrocytes, scattered microglia, parenchyBakshi e t al: S o litary In fla m m a to ry Brain Masses 9 Fig 2. Patient 1. Other MRI studies. (A) Frontal lesion, hypointense on sagittal non-contrast T1-WI. (B) Post-contrast axial T1-WI. Patchy] Neu intense enhancement. (C) Coronal T2-WI. Lesion progression, extensive involvement of the subcortical white matter. mal macrophages, and demyelination with relative axonal and oligodendroglial preservation. Management with prednisone (40 mg/day) led to clinical improvement and lesion size reduction (not shown). Over the next 8 years, there was no recurrence of the mass. Patien t 3: A 54-year-old man developed a generalized seizure. Computed tomography revealed an enhancing le­ sion in the frontal lobe, exerting minimal mass effect (not shown). On MRI, the mass was located in the frontal white matter and gray-white junction; it was hypointense on TlWI, hyperintense on T2-WI, and irregularly enhancing (Figs 3A, B). A stereotactic biopsy revealed demyelina­ tion of white matter with perivascular lymphocytes, reac­ tive astrocytosis, prominent perivascular and parenchymal lipid-laden macrophages, scattered microglia, and focal ar­ eas of necrosis. Cerebrospinal fluid findings are presented in Table 2. Despite a transient corticosteroid response (Fig 3C), enlargement of the mass followed 2 months later on MRI (Fig 3D). Two repeat biopsies, including an open biopsy, revealed similar changes; results of electron micro­ scopic and culture studies for fungi, parasites, viral inclu­ sion bodies, or other microorganisms were unremarkable. The lesion ultimately became atrophic and nonenhancing (not shown). Seven years after presentation, the clinical status and neuroimaging studies remained stable. P atien t 4: A 37-year-old woman developed a right hemi­ paresis. A CT scan revealed a nonenhancing, supraten­ torial hypodense lesion (Fig 4A) in the periventricu­ lar white matter and gray-white junction. On MRI, it was hypointense on Tl-W I and hyperintense on T2-WI, without mass effect or abnormal enhancement (Table 1). Cerebrospinal fluid findings are presented in Table 2. An open biopsy revealed demyelination of white matter with relative axonal and oligodendroglial preservation, 10 Journal o f N eu ro im ag in g Vol 8 No 1 January 1998 cate* perivascular lymphocytes, reactive astrocytes, scatters tom< microglia, and myelin-laden macrophages. Over the next ated 2 years, worsening hemiparesis and seizures coincident hype with enlargement of the mass partially responded to cod hanc ticosteroids. Over the next 17 years, seizures and hemi nodi paresis persisted. Serial MRI scans revealed encephalo hem malacia in the area of the prior mass, resulting in ex-vacu< the 1 dilatation of the lateral ventricle (Figs 4B, C). No nev ter.' lesions appeared, and two repeat biopsies were unreveal two ing. and Patient 5: A 43-year-old woman developed a generalize! Lab< seizure. A head CT revealed a homogeneously-enhancinj labo hypodense lesion without mass effect (Figs 5A, B) in th( gin, occipito-parietal lobar white matter and gray-white junc mun tion, extending to the cortex. On MRI, it was hypointensi on Tl-WI, hyperintense on T2-WI, and homogeneous! Path enhancing (Figs 5C-E). A stereotactic biopsy revealed abl pam normal white matter with perivascular lymphocytes, reac t \[m tive astrocytes, scattered microglia, and mild demyelina sca^ tion w ith rela tiv e axonal and oligod en droglia phaf preservation. A repeat biopsy revealed similar change! Management with prednisone (40 mg/day) led to clinics improvement and lesion size reduction on MRI (no Tabli shown). Eight years after presentation, with clinical stsj bility, MRI revealed a nonenhancing atrophic lesion (Fi Path 1 5F). 2 Su m m ary of Clinical M aterial: Our five patients, ages 1 to 66, developed seizures and/or hemiparesis, secondary ti 3 solitary inflammatory mass lesions that regressed ove months to years. Corticosteroid therapy was associate with improvement in each case. After 7-17 years, none o 5 the patients showed clinical evidence for a second c e n t o nervous system lesion, active infection, neoplastic diseaseIndex or multiple sclerosis. bands Table 1. Summary of Neuroimaging Findings Other CT/MRI Features MRI CT +C Ring, Nodular itient Age/Sex Unenhanced 1 19/F Hypodense 2 66/F Hypodense » Irreg 3 54/M Hypodense Homo, Irreg 4 37/F Hypodense None 5 43/F Hypodense Homo t +c Nodular i T Irreg Mild None None i T Homo, Irreg Mild None None i t N/A None None None Homo None None None TI i T2 T Mass Effect Ca+ Hemor Location None None None F, Perivent; White, G-W jn > cortex F, Perivent; White, G-W jn F, Lobar; White, G-W jn > cortex F-P-O, Perivent; White, G-W jn P-O, Lobar; White, G-W jn > cortex I = decreased signal; t = increased signal (vs. gray matter); +C = postcontrast enhancement; Ca+ = calcification; F = frontal; G-W jn = gray-white ||junction; Hemor = hemorrhagic component; Homo = homogeneous; Irreg = irregular; N/A = not available; O = occpital; P = parietal; Perivent j periventricular; White = supratentorial white matter. chy, tion was noted. Small, focal areas of necrosis were noted in only one patient (Patient 3). Vascular inflammation, hem­ orrhage, microglial nodules, inclusion bodies, neoplasia, and microorganisms were not present. Immunoperoxidase staining identified the perivascular lymphocytes to be pre­ dominantly T-cell (Patients 1, 3). Neuroimaging Fin d in g s: Neuroimaging features indi­ cated the possiblity of a neoplasm (Table 1). Computed red tiomography revealed a solitary hypodense lesion associ­ text ated with mild to no mass effect. On MRI, the lesions were lent hypointense on Tl-W I and hyperintense on T2-WI. En­ ;or- hancement was homogeneous/irregular (n = 3) or ring/ mi- nodular (n = 1). There was no evidence of calcification, alo- hemorrhage, cystic change or increased vascularity. All of cuo the lesions were located in the supratentorial white mat­ lew ter. Three lesions abutted the lateral ventricles; the other eal- two were lobar. Ultimately, the lesions became atrophic and nonenhancing on MRI. D iscussion Our patients presented with focal cerebral signs and symp­ toms, including seizures and hemiparesis, attributable to solitary supratentorial brain mass lesions that were iden­ tified on MRI and CT scans. The neuroimaging findings indicated the possibility of a neoplasm, prompting a bi­ opsy; however, an inflammatory, demyelinating process was revealed. The lesions involved the periventricular or lobar subcortical white matter with extension to the corticomedullary junction. They were diffusely hypodense on CT scans, hypointense on Tl-W I, and hyperintense on T2-WI, probably reflecting the inflammatory demyelinat­ ing nature of the lesions. Enhancement was seen in nearly all of the lesions on CT and MRI scans, with patterns that ranged from diffuse/homogeneous to irregular/ring-like. The abnormal contrast enhancement in these lesions most zed Laboratory Testing: Extensive CSF (Table 2) and other 'ing laboratory investigations did not disclose an infectious ori­ the gin, neoplastic disease, multiple sclerosis, or other autoim­ inc- mune origin. nse asly Pathologic Findings: Each of the lesions showed an in­ ab- flammatory process associated at least focally with demy^ac- elination. Perivascular lymphocytes, reactive astrocytosis, ina- scattered microglia, myelin-laden parenchymal macro­ lial phages and relative axonal and oligodendroglial preserva­ ges. ical not Table 2. Summary of CSF Findings WBC/ sta Patient RBC (% differential) Tig 4 (100L) <100 Glucose (mg/dl) Protein (mg/dl) 55 49 14 (100L) 67 38 1 2 <100 Negative Studies Cytology, Bact, Fung, TB, Obands, IgG, Crypt, VDRL, Lyme, Encephalitis panel Cytology, Bact, Fung, TB, Obands, IgG, Crypt, VDRL, Lyme, Encephalitis panel Cytology, Bact, Fung, TB, Obands, IgG, Crypt, VDRL, Lyme Cytology, Bact, Fung, TB, Obands, IgG, Crypt, VDRL, Encephalitis panel N/A s 19 80 51 <100 2 (52M, 44L, 4N) y to 3 >ver 26 <100 63 25 (84L, 16M) tted 4 e of 5 N/A N/A N/A N/A tral Bact = routine bacterial culture; Crypt = crytococcal antigen; CSF = cerebrospinal fluid; Encephalitis panel [31]; Fung = fungal culture; IgG = IgG ase. Index (CSF/serum); L = lymphocytes; Lyme = antibodies to Borrella burgdorferi; N = neutrophils; N/A = not available; Obands = oligoclonal bands; RBC = erythrocytes per high power field; TB = mycobacterial culture; VDRL = syphilis; WBC = white blood cells per high power field. Bakshi e t al: S o litary In fla m m a to ry Brain Masses - 11 Fig 3. Patient 3. Serial axial MRI. (A, B) Initial presentation. Posterior frontal mass involving the lobar white matter and gray-whitt junction, hypointense on T1-WI (not shown), homogeneously hyperintense on T2-WI (A); homogeneous and irregular enhancement (B| (C) Three months after presentation. Corticosteroid therapy led to a marked reduction in the amount of enhancement. (D) Five month! after presentation. Clinical deterioration. Recurrent, intense areas of enhancement in the dorsal frontal lobe and new areas of enhance! ment in the anterior frontal lobe. likely reflects compromise of the blood-brain-barrier caused by active inflammation. Consistent with this hy­ pothesis, the abnormal enhancement correlated with clini­ cal worsening and resolved with corticosteroid therapy or clinical remission. Ultimately, the lesions decreased in size, became atrophic and failed to enhance. The initial neuroimaging findings of a single large enhancing supra­ tentorial mass lesion raised the suspicion for a neoplasm, prompting a biopsy. Solitary inflammatory lesions should be added to the differential diagnosis for lesions with simi­ lar clinical and neuroimaging findings. These lesions bear neuroimaging similarities to those of Kepes ,16 whose 28 of 31 patients developed tumor-like, single, solitary, corticosteroid-responsive demyelinating brain masses. However, pathologically, the masses showed prominent demyelination with associated inflammation In contrast, the current cases were characterized more b] inflammation, resembling a leukoencephalitis, with the as sociated demyelination being less prominent and with oli godendroglia being preserved. Other white matter inflaml matory demyelinating disorders occasionally resemble neoplasms on MRI or CT .1-15 For example, patients witl multiple sclerosis may develop large plaques, leading t( biopsy .1-10 These lesions share many of the neuroimaginf and pathologic features of the present cases .2,3,5,8 How ever, our patients clearly did not meet the diagnostic cri teria for multiple sclerosis .17 A second lesion was no Fig 5. no found by longitudinal evaluation. Acute disseminated en on gray-v (D = c atroph cepfn tures patho and o ings £ tracra bear 1 follov tients Barr a rolog neuro koenc forms Fig 4. Patient 4. CT: (A) Nonenhancing, hypodense lesion involving the periventricular, subcortical white matter and gray-whitfor Lyi junction. MRI: (B) Eight years after presentation. Encephalomalacia within the area of the prior mass, associated ex-vacuo dilatation of lateral ventricle. (C) Thirteen years after presentation. Stable lesion. :s • ■ thtand p; 12 Journal o f N eu ro im ag in g Vol 8 No 1 January 1998 ved ion. ; by asoliimLble vith 5 to ^ing owcrinot Fig 5. Patient 5. CT: (A, B) Initial presentation: Left occipito-parietal homogeneously enhancing lesion without mass effect (hypodense non-contrast images, not shown). MRI: (C-E) Initial presentation: Lobar white matter and gray-white junction lesion, extending to the en- on gray-white junction; (C) Hypointense on T1-WI, homogeneously enhancing (not shown). (D, E) Hyperintense on T2-WI (proton density) (D = axial; E = coronal); hyperintensities resemble a peritumoral vasogenic edema pattern. (F) Nine years after presentation: Smaller, atrophic lesion; ex-vacuo ventricular dilatation; nonenhancing (not shown). cephalomyelitis (ADEM ) may show neuroimaging fea­ tures indistinguishable from a neoplasm .8,13,14 While pathologic similarities do exist between ADEM lesions and our cases ,8 the clinical course and neuroimaging find­ ings are not consistent with typical ADEM; multiple in­ tracranial lesions are typically noted on MRI .18 Our cases bear histologic similarities to a leukoencephalitis that may follow Epstein-Barr virus infection .19,20 One of our pa­ tients (Case 2) developed serologically confirmed EpsteinBarr virus infection 6 months before the onset of the neu­ rologic symptoms. However, the clinical course and neuroimaging findings of post-Epstein-Barr virus leu­ koencephalitis are not similar to our cases .20 Bacterial forms of leukoencephalitis, such as Whipple’s disease 21-24 or Lyme disease 25 can be excluded by the neuroimaging and pathologic findings. Rasmussen’s chronic encephalitis is similar clinically to the current cases 26,27 However, this entity can be excluded by the pathologic 26 and neuroim­ aging27-29 findings. Similarities exist between our cases and a recent series of focal, corticosteroid-responsive, inflammatory demyelinating, contrast-enhancing brain masses .30 However, each of these patients developed new, separate, symptom­ atic brain lesions several months later that were diagnosed as primary central nervous system lymphoma. This entity is excluded by the longitudinal follow-up failing to reveal lymphoma in our cases. In addition, many of these “sen­ tinel lesions of lymphoma” were located in deeper brain regions, such as the brain stem, internal capsule, and hy­ pothalamus, unlike the current cases. The etiology of these unusual, solitary, supratentorial, inflammatory demyelinating, space-occupying lesions re­ mains speculative. The significant improvement after cor­ ticosteroid therapy, followed by the ultimate regression of Bakshi e t al: S o litary In fla m m a to ry Brain Masses 13 the masses, suggests that this syndrome may represent one or more inflammatory disorders, such as a solitary form of a syndrome similar to ADEM or multiple sclerosis or an undetermined insidious infection. The clinical and patho­ logic findings favored a diagnosis of inflammatory leu­ koencephalitis; however, the initial neuroimaging findings indicated the possibility of a neoplasm. Because of the nonspecific neuroimaging and pathologic features and an uncertain etiology, this syndrome may be referred to sim­ ply as “leukoencephalitis.” R eferen ces 1. Prockop LD, Heinz ER. Demyelinating disease presenting as an intracranial mass lesion. Arch Neurol 1965;13:559564 2. Hunter SB, Ballinger WE, Rubin JJ. Multiple sclerosis mimicking primary brain tumor. Arch Pathol Lab Med 1987;111:464-468 3. 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AJR 1992;158:1329-1332 29. Zupanc ML, Handler EG, Levine RL, et al. Rasmussen encephalitis: epilepsia partialis conitinua secondary to chronic encephalitis. Pediatr Neurol 1990;6:397-401 30. Alderson L, Fetell MR, Sisti M, Hochberg F, Cohen M, Louis DN. Sentinel lesions of primary CNS lymphoma, J Neurol Neurosurg Psychiatry 1996;60:102-105 31. CSF and serum viral antibody testing was negative for ac-1 tive infection with Eastern, St. Louis, and Western en­ cephalitis, La Crosse, Adenovirus, Coxsackie, Echovirus, I Herpes Simplex, Influenza, Lymphocytic Choriomeningitis! Mumps, Rubeola, or Varicella-Zoster viruses (Specialty Laboratories, Santa Monica, CA)