80 MR Imaging of Cerebral Gumma Geoffrey A. Agrons , 1 Sao Sung Han, 1 Michael A. Husson , 2 and Frederick Simeone 3 Cerebral gumma, as a manifestation of neurosyphilis, is unu sual. The CT and MR findings in a patient with a surgically proved frontal convexity granuloma and strongly positive syphilis serologies is presented. To our knowledge, the MR appearance of a syphilitic gumma has not been described previously in t he sci entific literature. Case Report A 43-year-old woman was brought to t he emergency room fo ll ow- ing a generalized tonic-cloni c seizure. While in the emergency room, she suffered a second seizure, which began with right facial twitching and progressed to a generali zed convulsion. After the sei zure, the patient experi ence d no focal neurologic defi cits, and a neurol og ic examination di sclosed no motor or sensory abnormaliti es. Laboratory studies were within normal li mits. The pat ient had no history of neurologic disease, was on no medications, and gave no history of usi ng eth anol or drugs. A head CT scan reveal ed a densely enhancing left frontal convexity mass with surroundi ng edema, associated with mil d di splacement of the fa lx cerebri to the right (Figs. 1A and 1B). For MR imaging a General El ectric 1.5-T Signa system wi th a spin- echo pulse sequence was used. Noncontrast T1 -wei ghted images of the brain , 650 /30/1 ( TR/TE{excitati ons) , showed a 1 em x 1.2 em per ipherall y situated anteri or frontal mass with a peripheral rim of increased signal intensity and a central area of diminished signal intensity (Fi g. 1 C). Th ere was en hancement of the central portion of th e mass following administration of gadopentetate dimeg lumine (Fig. 1D). T2-weighted images demonstrated l esion hypointensity with surrounding edema (Fi g. 1 E) . An en bloc resecti on of a 2.5-cm piece of frontal cortex yielded a 1-cm rounded tan nodul e of rubbery consistency. Final pathologic results demonstrated a cortical nodule composed of a central fibrotic area surrounded by a rather extensi ve perivascular infiltration of lymphocytes and pl asma ce ll s (Fig. 1 F) , and further characterized by neuronal loss and associated adhesive arachnoiditis. A Steiner si lver stain was performed in an attempt to identify Treponema pallidum spirochetes, but no organi sms coul d be found. Th e hi stologic features of the nod ul e were thought to be consistent with, but not diagnos ti c of, a syphilitic gumma. The pathologic findings prompted serologic test ing of the patient, revealing a strongly positive rapid plasma reagin at 1:256, as we ll as a positive microhemagglutination assay for Treponema pallidum. The patient's HI V status was not determined. Discussion Meningitis, usually asymptomatic initially, is the final com- mon pathway for the later symptomatic forms of neuro- syphilis: parenchymatous and meningovascular [1]. The pathophysiology of the transformation from early CNS inva- sion by Treponema pallidum to chronic parenchymatous dis- ease has not been elucidated. Previous descriptions of CT findings in neurosyphilis com- prise a spectrum of parenchymal abnormalities. Extensive areas of diminished frontal lobe white matter attenuation with cortical atrophy have been described, as well as multiple posterior fossa infarctions [2]. A widespread hemispheric white matter lesion with mass effect, simulating a low-grade infiltrating primary tumor, has been demonstrated in a hemi- paretic patient with positive syphilis serologies and confirma- tory biopsy [3] . A densely enhancing focal lesion in the pons and midbrain resolved with penicillin therapy, and was pre- sumed to represent a syphilitic gumma [4]. Similarly, a case of multiple cerebral gummata involving the frontotemporal area and anterior corpus callosum has been reported, with regression upon penicillin treatment [5]. A cerebellopontine angle mass, mimicking an acoustic neuroma, proved to be consistent with a gumma at surgical extirpation [6]. Recently, MR and CT features have been presented in three cases of meningovascular syphilis [7], consisting of multiple small in- farcts affecting gray and white matter in scattered vascular territories , ind istinguishable from other vasculitides. In t he present case, the physical basis for the observed rim of hyperintensity on unenhanced short TR images (with lesion hypointensity on long TR scans) is not clear. Pathologic evaluat ion demonstrated no evidence of blood products, ex- clud i ng T1 and T2 shortening by paramagnetic methemoglo- bin as a possible mechanism. In mature abscesses, capsule walls exhibiting similar signal behavior have been described, and varying degrees of T2 st)ortening on long TR studies have been observed in parenchymal granulomatous disease. This phenomenon has been attributed to the production of intracellular paramagnetic f ree radicals during phagocytosis [8]. Cerebral gumma has become exceedingly rare in the United States, illustrat ed by t he fact t hat a seropositive pat ient with Received April 12, 1990; revi sion requested June 25, 1990; revi si on 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, Pennsyl va ni a Hospital, Phil adelphia, PA 19107. 3 Department of Neurosurgery, Pennsyvlani a Hospital, Philadelphia, PA 19107. AJNR 12:80- 81 , January/February 1991 0195-6108/ 91 / 1201 - 0080 © Ameri can Society of Neuroradiology
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80
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 neurosyphilis, is unusual. The CT and MR findings in a patient with a surgically proved frontal convexity granuloma and strongly positive syphilis serologies is presented. To our knowledge, the MR appearance of a syphilitic gumma has not been described previously in the scientific literature.
Case Report
A 43-year-old woman was brought to the emergency room following a generalized tonic-clonic seizure. While in the emergency room, she suffered a second seizure, which began with right facial twitching and progressed to a generalized convulsion. After the seizure, the patient experienced no focal neurologic deficits, and a neurologic examination disclosed no motor or sensory abnormalities. Laboratory studies were within normal limits. The patient had no history of neurologic disease, was on no medications, and gave no history of using ethanol or drugs.
A head CT scan revealed a densely enhancing left frontal convexity mass with surrounding edema, associated with mild displacement of the falx cerebri to the right (Figs. 1 A and 1 B).
For MR imaging a General Electric 1.5-T Signa system with a spinecho pulse sequence was used. Noncontrast T1 -weighted images of the brain , 650/30/1 (TR/TE{excitations), showed a 1 em x 1.2 em peripherally situated anterior frontal mass with a peripheral rim of increased signal intensity and a central area of diminished signal intensity (Fig. 1 C). There was enhancement of the central portion of the mass following administration of gadopentetate dimeglumine (Fig. 1 D). T2-weighted images demonstrated lesion hypointensity with surrounding edema (Fig. 1 E).
An en bloc resection of a 2.5-cm piece of frontal cortex yielded a 1-cm rounded tan nodule of rubbery consistency. Final pathologic results demonstrated a cortical nodule composed of a central fibrotic area surrounded by a rather extensive perivascular infiltration of lymphocytes and plasma cells (Fig . 1 F), and further characterized by neuronal loss and associated adhesive arachnoiditis. A Steiner silver stain was performed in an attempt to identify Treponema pallidum spirochetes, but no organisms could be found. The histologic features of the nodule were thought to be consistent with , but not diagnostic of, a syphilitic gumma.
The pathologic findings prompted serologic testing of the patient , revealing a strongly positive rapid plasma reagin at 1 :256, as well as a positive microhemagglutination assay for Treponema pallidum. The patient's HIV status was not determined.
Discussion
Meningitis, usually asymptomatic initially, is the final common pathway for the later symptomatic forms of neurosyphilis: parenchymatous and meningovascular [1]. The pathophysiology of the transformation from early CNS invasion by Treponema pallidum to chronic parenchymatous disease has not been elucidated.
Previous descriptions of CT findings in neurosyphilis comprise a spectrum of parenchymal abnormalities. Extensive areas of diminished frontal lobe white matter attenuation with cortical atrophy have been described, as well as multiple posterior fossa infarctions [2]. A widespread hemispheric white matter lesion with mass effect, simulating a low-grade infiltrating primary tumor, has been demonstrated in a hemiparetic patient with positive syphilis serologies and confirmatory biopsy [3] . A densely enhancing focal lesion in the pons and midbrain resolved with penicillin therapy, and was presumed to represent a syphilitic gumma [4]. Similarly, a case of multiple cerebral gummata involving the frontotemporal area and anterior corpus callosum has been reported, with regression upon penicillin treatment [5] . A cerebellopontine angle mass, mimicking an acoustic neuroma, proved to be consistent with a gumma at surgical extirpation [6] . Recently , MR and CT features have been presented in three cases of meningovascular syphilis [7], consisting of multiple small infarcts affecting gray and white matter in scattered vascular territories , indistinguishable from other vasculitides.
In the present case, the physical basis for the observed rim of hyperintensity on unenhanced short TR images (with lesion hypointensity on long TR scans) is not clear. Pathologic evaluation demonstrated no evidence of blood products, excluding T1 and T2 shortening by paramagnetic methemoglobin as a possible mechanism. In mature abscesses, capsule walls exhibiting similar signal behavior have been described, and varying degrees of T2 st)ortening on long TR studies have been observed in parenchymal granulomatous disease. This phenomenon has been attributed to the production of intracellular paramagnetic free radicals during phagocytosis [8] .
Cerebral gumma has become exceedingly rare in the United States, illustrated by the fact that a seropositive patient with
Received April 12, 1990; revision 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 material , 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 processesa cerebral neoplasm and asymptomatic neurosyphilis-than a gumma [9] . Differential considerations for an enhancing parenchymal nodule are extensive, and include glioma, metastasis, tuberculosis , and sarcoid and fungal infections, among others. The radiologic findings , then, are nonspecific, and anatomic localization is of little help [6]. Thus, the diagnosis remains one of clinical and laboratory synthesis.
REFERENCES
1. Adams RD, Victor M. Principles of neurology. New York: McGraw-Hill , 1977:639-646
2. Ganti SR , Cohen M, Sane P, et al. Computed tomography of cerebral syphilis. J Comput Assist Tomogr 1981 ;5:345-347
3. Kulla L, Russell JA, Smith TW, et al. Neurosyphilis presenting as a focal mass lesion: a case report. Neurosurgery 1984;14 :234-237
4. Godt P, Stoeppler L, Wischer U, Schroeder HH. The value of computed tomography in cerebral syphilis. Neuroradiology 1979;18:197-200
5. Punt J. Multiple cerebral gummata: case report. J Neurosurg 1983;58 : 959-961
6. Eltomey AA, Olin MS, Roberts MP. Cerebellopontine angle gumma. Neurosurgery 1984;15:252-253
7. Holland BA, Perrett LV, Mills CM. Meningovascular syphilis : CT and MR findings. Radiology 1986;158:439-442
8. Sze G, Zimmerman RD. The magnetic resonance imaging of infections and inflammatory diseases. Radio/ Clin North Am 1988;26 :839-859
9. Adams RD, Victor M. Principles of neurology. New York: McGraw-Hill , 1977:601
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