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Figure 1. A contrast-enhanced computed tomographic scan of the upper abdomen reveals enlargement of the spleen (arrows).

Jeffrey A. Nelson and Albert A. Nemcek, Jr. Department of Medicine, Rush Medical College; and Department o] Radiology, Northwestern Memorial Hospital. Chicago, Illinois

References I. Burgdorfer W. Discovery of the Lyme disease spirochete and its relation to tick vectors. Y J Bioi Med 1984;57:515-20. 2. Steere AC, Bartenhagen NH, Craft lE, et al. The early clinical manifestations of Lyme disease. Ann Intern Med 1983;99:76-82. 3. Steere AC, Malawista SE, Hardin lA. Ruddy S. Askenase PW. Andiman WA. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med 1977;86:685-98. 4. Malane MS, Grant-Kels 1M. Feder HM. Lugar SW. Diagnosis of Lyme

Central Nervous System Tuberculoma Presenting as a Cavernous Sinus Tumor SIR-CNS tuberculoma is the most common etiology of granulomatous pathological reactions in the CNS [1-3]. Other condiThe opinions or assertions herein are the private views of the authors and are not to be construed as reflecting the views of the U.S. Departmen t of the Army or the U.S. Department of Defense. Correspondence: Dr. Joseph T. Morris. U.S. Army Medical Corps, Infectious Disease Service. Brooke Army Medical Center, Fort Sam Houston, Texas 78234-6200.

Clinical Infectious Diseases 1992;15:181-2 This article is in the public domain.

disease based on dermatologic manifestations. Ann Intern Med

1991;114:490-8. 5. Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme disease: meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53. 6. Cools L, Osteaux M. Divano L, Jeanmaut L. Prediction of splenic volume by a simple CT measurement: a statistical study. J Cornput Assist Tomogr 1983;7:426-30. 7. Nelson lA. Bankowski Ml, Newton BJ, eta!' Detection ofantibodies in late Lyme disease. J Infect Dis 1990; 161:1034-5. 8. Ma B. Christen B, Leung D, Vigo-Pelfrey C. Serodiagnosis of Lyme borreliosis by Western immunoblot: reactivity of various significant antibodies against Borrelia burgdorferi. J Clin Microbial 1992:30

370-6. 9. Asbrink E. Olsson I. Clinical manifestations of erythema chronicum migrans Afzelius in 161 patients. Acta Derrn Venereal 1985:65:43-

52. 10. Reik L. Steere AC Bartenhagen NH, Shope RE, Malawista SE. Neurologic abnormalities of Lyme disease. Medicine (Baltimore) 1979;58: 281-94.

tions that cause granulomatous pathological reactions include sarcoidosis, fungal infections (cryptococcosis, aspergillosis, and mucormycosis), toxoplasmosis, collagen vascular diseases (rheumatoid arthritis and granulomatous vasculitis), and the presence of foreign bodies (surgical sutures). We describe a patient whose eNS tuberculoma was found during evaluation for a cavernous sinus tumor. A 42-year-old Filipino woman with an 8-year history of migraines presented to her neurologist in July 1991 with a complaint of numbness of the entire left face, a left sharp retroorbital headache that was different from her usual migraines, and numbness of the left halfof her tongue. A neurological examination revealed only a left fifth cranial nerve palsy. Contrast-en-

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tance ofobtaining a travel history in the evaluation of patients to facilitate the consideration of Lyme borreliosis.

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In countries in which intracranial tuberculomas account for a significant percentage of intracranial mass lesions, diagnosis is made on clinical grounds and is supported by results ofan intravenous contrast-enhanced computed tomographic scan of the head that may demonstrate an enhancing mass lesion( s) surrounded by marked edema [2, 5-7]. Treatment with antituberculous agents that penetrate the CNS has been found to be superior to surgical intervention [2, 8]. Chemotherapy with antituberculous agents should be started on the basis of a strong clinical suspicion; treatment should not be delayed pending results of histologic studies [8]. Systemic corticosteroids can be used to reduce increased intracranial pressure caused by the intracranial lesions [2, 8, 9]. Although the intracranial tuberculoma was not microbiologically confirmed, the results of the histopathological examination, our patient's history, and the lack of further neurological deterioration once therapy with antituberculous agents was begun support our diagnosis of CNS tuberculoma for this patient. Physicians should be more aware of this extrapulmonary manifestation of Mycobacterium tuberculosis disease since infection with this pathogen is increasing in the United States.

Joseph T. Morris and M. Patricia Joyce Infectious Disease Service. Department of Medicine. Brooke Army Medical Center. Fort Sam Houston. Texas

References l. Gupta RK. lena A, Singh AK. Sharma A, Puri Y. Gupta M. Role of magnetic resonance (MR) in the diagnosis and management of intracranial tuberculomas. Clin Radiol 1990;41: 120-7. 2. Harder E. Al-Kawi M, Carney P. Intracranial tuberculoma: conservative management. Am J Med 1983;4:570-6. 3. Weisberg LA. Granulomatous diseases of the CNS as demonstrated by computerized tomography. Comput Radiol 1984;8:309-17. 4. Bishburg E. Sunderam G, Reichman LB. et al. Central nervous system tuberculosis with the acquired immunodeficiency syndrome and its related complex. Ann Intern Med 1986; I 05:21O. 5. Kingsley DP, Hendrickse WA, Kendall BE, Swash M. Singh Y. Tuberculous meningitis: role of CT in management and prognosis. J Neurol Neurosurg Psychiatry 1987;50:30-6. 6. Bagga A. Kaira Y, Ghai OP. Intracranial tuberculoma: evaluation and treatment. Clin Pediatr (Phila) 1988;27:487-90. 7. Loizou LA, Anderson M. Intracranial tuberculomas: correlation of computerized tomography with c1inico-pathological findings. Q J Med

1982;51: 104-14. 8. Leonard 1M, Des Prez RM. Tuberculous meningitis. Infect Dis Clin North Am 1990;4:769-87. 9. Chambers ST. Hendricks WA, Record C. Rudge P, Smith H. Paradoxical expansion of intracranial tuberculomas during chemotherapy. Lancet

1984;2: 181-3.

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hanced magnetic resonance imaging of her brain demonstrated a circumscribed lesion along the left cavernous sinus region that measured 2 X 2 X 1.5 em and inflammatory changes in the proximal part of the left fifth cranial nerve. This solitary cavernous sinus lesion was believed to represent a small meningioma. An unenhanced computerized tomographic (CT) scan of her head was normal. The patient declined neurosurgery at that time, and in early October 1991, she presented again with vertigo, worsening of the left retroorbital headache, blurred vision (left eye worse than the right eye), decreased visual acuity over the previous 4 days, photophobia, excess lacrimation from the left eye, and ptosis of the left eye. Physical examination was significant for left fifth and sixth nerve palsies, ptosis of the left eye, and absence of the left corneal reflex. An angiogram revealed that the mass was avascular, a finding thought to be consistent with a schwannoma. A diagnosis of a meningioma or schwannoma was made, and the patient was taken to the operating room. The mass could not be resected entirely, and the intraoperative frozen section was consistent with a meningioma. The patient's postoperative course was significant only for mild slurring of her speech and a left central seventh cranial nerve palsy. The final pathological examination of the excised tissue revealed a caseating granulomatous plaque and multinucleated giant cells. Special stains for fungal elements and acid-fast bacilli were negative. Ascertainment of further history revealed that the patient had a positive PPD test when she emigrated from the Philippines in 1975. A chest radiograph at that time showed no evidence of active pulmonary tuberculosis, and chemoprophylaxis with isoniazid was not given. A chest radiograph obtained during her preoperative evaluation was unremarkable. Her serology for human immunodeficiency virus was negative. Smears of first-morning specimens of sputum and urine were negative for acid-fast bacilli, and all cultures were negative at 6 weeks. Therapy with isoniazid (300 mg/d), rifampin (600 mg/ d), pyrazinamide (25 mg/[kg· d]), and pyridoxine (50 mg/d) for an intracranial tuberculoma was begun. Since discharge, her left seventh cranial nerve palsy has persisted. Additional neurological deficits have not been noted on physical examination. Tuberculoma as an extrapulmonary manifestation oftuberculosis is thought to be a result of hematogenous spread from elsewhere in the body. In developing countries, tuberculomas constitute 20%-30% of brain tumors compared with < 1% of brain tumors in the United States [I, 2]. According to a report by Bishburg et al. [4], the incidence of intracranial tuberculomas may be increasing in the United States because of the effect of human immunodeficiency virus infection on the clinical expression of CNS tuberculosis. Symptoms of systemic illness and meningeal irritation may be absent since only -... 30% of patients have evidence oftuberculosis outside the CNS [5].

Central nervous system tuberculoma presenting as a cavernous sinus tumor.

CIO 1992; 15 (July) 181 Correspondence Figure 1. A contrast-enhanced computed tomographic scan of the upper abdomen reveals enlargement of the sple...
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