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MR Imaging of Cerebral Gumma

Geoffrey A. Agrons,1 Sao Sung Han ,1 Michael A. Husson,2 and Frederick Simeone3

Cerebral gumma, as a manifestation of , is Discussion unusual. The CT and MR findings in a patient with a surgically Meningitis, usually asymptomatic initially, is the final com­ proved frontal convexity and strongly positive mon pathway for the later symptomatic forms of neuro­ serologies is presented. To our knowledge, the MR syphilis: parenchymatous and meningovascular [1]. The appearance of a syphilitic gumma has not been described pathophysiology of the transformation from early CNS inva­ previously in the scientific literature. sion by Treponema pallidum to chronic parenchymatous dis­ ease has not been elucidated. Case Report Previous descriptions of CT findings in neurosyphilis com­ prise a spectrum of parenchymal abnormalities. Extensive A 43-year-old woman was brought to the emergency room follow­ areas of diminished frontal lobe white matter attenuation with ing a generalized tonic-clonic seizure. While in the emergency room, cortical atrophy have been described, as well as multiple she suffered a second seizure, which began with right facial twitching posterior fossa infarctions [2]. A widespread hemispheric and progressed to a generalized convulsion. After the seizure, the white matter lesion with mass effect, simulating a low-grade patient experi enced no focal neurologic defi cits, and a neurologic infiltrating primary tumor, has been demonstrated in a hemi­ examination disclosed no motor or sensory abnormalities. Laboratory paretic patient with positive syphilis serologies and confirma­ studies were within normal li mits. The patient had no history of tory biopsy [3]. A densely enhancing focal lesion in the pons neurologic disease, was on no medications, and gave no history of using eth anol or drugs. and midbrain resolved with penicillin therapy, and was pre­ A head CT scan revealed a densely enhancing left frontal convexity sumed to represent a syphilitic gumma [4]. Similarly, a case mass with surrounding edema, associated with mild displacement of of multiple cerebral gummata involving the frontotemporal the falx cerebri to the right (Figs. 1 A and 1 B). area and anterior corpus callosum has been reported, with For MR imaging a General Electric 1.5-T Signa system with a spin­ regression upon penicillin treatment [5]. A cerebellopontine echo pulse sequence was used. Noncontrast T1 -weighted images of angle mass, mimicking an acoustic neuroma, proved to be the brain , 650/30/1 (TR/TE{excitations), showed a 1 em x 1.2 em consistent with a gumma at surgical extirpation [6]. Recently, peripherally situated anteri or frontal mass with a peripheral rim of MR and CT features have been presented in three cases of increased signal intensity and a central area of diminished signal meningovascular syphilis [7], consisting of multiple small in­ intensity (Fig. 1C). There was enhancement of the central portion of farcts affecting gray and white matter in scattered vascular the mass following administration of gadopentetate dimeg lumine (Fig. 1 D). T2-weighted images demonstrated lesion hypointensity with territories, indistinguishable from other vasculitides. surrounding edema (Fig. 1 E). In the present case, the physical basis for the observed rim An en bloc resection of a 2.5-cm piece of frontal cortex yielded a of hyperintensity on unenhanced short TR images (with lesion 1-cm rounded tan nodule of rubbery consistency. Final pathologic hypointensity on long TR scans) is not clear. Pathologic results demonstrated a cortical nodule composed of a central fibrotic evaluation demonstrated no evidence of blood products, ex­ area surrounded by a rather extensi ve perivascular infiltration of cluding T1 and T2 shortening by paramagnetic methemoglo­ lymphocytes and plasma cells (Fig . 1 F), and further characterized by bin as a possible mechanism. In mature abscesses, capsule neuronal loss and associated adhesive arachnoiditis. A Steiner silver walls exhibiting similar signal behavior have been described, stain was performed in an attempt to identify Treponema pallidum and varying degrees of T2 st)ortening on long TR studies spirochetes, but no organi sms could be found. The histologic features have been observed in parenchymal granulomatous disease. of the nodule were thought to be consistent with, but not diagnostic of, a syphilitic gumma. This phenomenon has been attributed to the production of The pathologic findings prompted serologic testing of the patient, intracellular paramagnetic free radicals during phagocytosis revealing a strongly positive rapid plasma reagin at 1 :256, as well as [8] . a positive microhemagglutination assay for Treponema pallidum. The Cerebral gumma has become exceedingly rare in the United patient's HI V status was not determined. States, illustrated by the fact that a seropositive patient with

Received April 12, 1990; revi sion requested June 25, 1990; revision received August 7, 1990; accepted August 13, 1990. ' Department of Radiology, Pennsylvania Hospital, 8th and Spruce Sts., Philadelphia, PA 19107. Address reprint requests to G. A. Agrons. 2 Department of Pathology, Pennsylvania Hospital, Philadelphia, PA 19107. 3 Department of Neurosurgery, Pennsyvlania Hospital, Philadelphia, PA 19107. AJNR 12:80- 81 , January/February 1991 0195-6108/91 / 1201 - 0080 © American Society of Neuroradiology AJNR :12 , January/February 1991 MR OF CEREBRAL GUMMA 81

D E F

Fig. 1.-43-year-old woman with cerebral gumma as a manifestation of neurosyphilis. A and 8, Axial CT sections through high frontal convexities, before and after IV administration of contrast materi al, show enhancing mass with extensive surrounding edema. C, Unenhanced axial T1-weighted (650/30) MR image of the brain shows left frontal mass with hypointense core, irregular hyperintense rim, and surrounding vasogenic edema. · D, Contrast-enhanced T1-weighted (650/30) axial MR image shows enhancement of the nodule's central portion. E, T2-weighted (2500/80) MR image reveals diminished signal intensity of the nodule. F, High-power photomicrograph of cortical nodule reveals prominent perivascular chronic inflammatory infiltrate by lymphocytes and plasma cells. (H and E)

an intracerebral mass is more likely to have two processes­ 2. Ganti SR , Cohen M, Sane P, et al. Computed tomography of cerebral a cerebral neoplasm and asymptomatic neurosyphilis-than syphilis. J Comput Assist Tomogr 1981 ;5:345-347 3. Ku lla L, Russell JA, Smith TW, et al. Neurosyphilis presenting as a focal a gumma [9]. Differential considerations for an enhancing mass lesion: a case report. Neurosurgery 1984;14 :234-237 parenchymal nodule are extensive, and include glioma, me­ 4. Godt P, Stoeppler L, Wischer U, Schroeder HH. The value of computed tastasis, , and sarcoid and fungal infections, tomography in cerebral syphilis. Neuroradiology 1979;18:197-200 among others. The radiologic findings, then, are nonspecific, 5. Punt J. Multiple cerebral gummata: case report. J Neurosurg 1983;58 : 959-961 and anatomic localization is of little help [6]. Thus, the diag­ 6. Eltomey AA, Olin MS, Roberts MP. Cerebellopontine angle gumma. Neu­ nosis remains one of clinical and laboratory synthesis. rosurgery 1984;15:252-253 7. Holland BA, Perrett LV , Mills CM . Meningovascular syphilis: CT and MR findings. Radiology 1986;158:439-442 REFERENCES 8. Sze G, Zimmerman RD . The magnetic resonance imaging of infections and inflammatory diseases. Radio/ Clin North Am 1988;26 :839-859 1. Adams RD , Victor M. Principles of neurology. New York: McGraw-Hill, 9. Adams RD , Victor M. Principles of neurology. New York: McGraw-Hill, 1977:639-646 1977:601