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CASE REPORT |
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Year : 2023 | Volume
: 3
| Issue : 1 | Page : 136-138 |
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Bilateral third and fourth cranial nerve palsy presenting secondary to central nervous system tuberculoma: A rare case report
Arumugam Balraj, Aditya Anand
Department of Neuro-Ophthalmology, Aravind Eye Hospital, Pondicherry, India
Date of Submission | 15-Aug-2022 |
Date of Acceptance | 28-Oct-2022 |
Date of Web Publication | 20-Jan-2023 |
Correspondence Address: Arumugam Balraj Aravind Eye Hospital, Thavalakuppam, Pondicherry - 605 007 India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ijo.IJO_2015_22
Central nervous system (CNS) tuberculoma can have variable presentations depending on the site and number of tuberculomas. We report a rare case of a 48-year-old male presenting with ptosis and binocular double vision. Clinical examination revealed bilateral third-nerve palsy and fourth-nerve palsy with nystagmus. Magnetic resonance imaging (MRI) of the brain revealed ring-enhancing lesion in the dorsal midbrain, suggestive of tuberculoma. Radiological search for tuberculous foci in other internal organs proved pulmonary tuberculosis. Mantoux was positive, confirming the exposure to tuberculous bacilli. He was started on low-dose steroids along with antitubercular therapy (ATT). There was no improvement after continuing ATT for one-and-a-half years. Thus, the prognosis of CNS tuberculoma is related to the timing of initiating appropriate therapy. Delays in diagnosis and treatment will result in poor prognoses and severe neurological sequelae.
Keywords: Fourth nerve palsy, midbrain, oculomotor nerve palsy, ptosis, tuberculoma
How to cite this article: Balraj A, Anand A. Bilateral third and fourth cranial nerve palsy presenting secondary to central nervous system tuberculoma: A rare case report. Indian J Ophthalmol Case Rep 2023;3:136-8 |
How to cite this URL: Balraj A, Anand A. Bilateral third and fourth cranial nerve palsy presenting secondary to central nervous system tuberculoma: A rare case report. Indian J Ophthalmol Case Rep [serial online] 2023 [cited 2023 Feb 1];3:136-8. Available from: https://www.ijoreports.in/text.asp?2023/3/1/136/368205 |
Tuberculosis remains a significant health problem in developing countries like India. Intracranial tuberculoma accounts for 5%–8% of space-occupying lesions in the brain. They are usually located in the cerebral or cerebellar hemisphere due to high blood supply to these areas, though the brain stem is an uncommon location.[1] This report documents a rare entity of bilateral third- and fourth-nerve palsy presenting secondary to central nervous system (CNS) tuberculoma.
Case Report | |  |
A 48-year-old male presented with drooping of the right eyelid for the past three months and drooping of the left eyelid for the past one month, associated with history of binocular diplopia and restricted extraocular movements, and also had a history of 5-kg weight loss in the last two months. On examination, best-corrected visual acuity (BCVA) in both eyes was 6/18. He had chin elevation. On ocular examination, both eyes showed severe ptosis with restriction of extraocular movements in all gazes except abduction [Figure 1]. There was divergent squint, and convergence of both eyes were absent. Horizontal nystagmus was present in our case, which was low in amplitude and frequency. Pupil was reacting sluggishly to both direct and consensual in both eyes. Anterior segment revealed immature cataract in both eyes. Fundus was normal in both eyes. Other cranial nerves were intact. Sensory and motor examination was normal. There was no focal neurological deficit. No cerebellar signs. Vestibular ocular reflex was preserved in our patient. | Figure 1: Extraocular movements showing restriction of all movements in all gazes except abduction in both eyes
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A definitive diagnosis of bilateral third- and fourth-nerve palsy was made. Both plain and contrast-enhanced magnetic resonance imaging(MRI) with MR angiography of the brain was ordered. It showed multiple ring enhancing lesions in the supratentorial and infratentorial neuroparenchyma (left frontal lobe and right cerebellum) and brainstem predominantly in midbrain, suggestive of tubercular granuloma [Figure 2]. MR spectroscopy (MRS) showed high peak of lipids, increased choline, low N-acetyl aspartate (NAA), and creatinine with choline/creatinine ratio >1, which confirmed tuberculoma. A radiological search for tuberculous foci in other internal organs proved pulmonary tuberculosis [Figure 3]. Mantoux test was positive, confirming the exposure to tuberculous bacilli. HIV testing returned negative, thereby ensuring that he was an immunocompetent individual. He was started on low-dose steroids along with anti-tubercular therapy (ATT) AKT 4 which is a combination of ethambutol hydrochloride 1.1 gm, isoniazid 300 mg, pyrazinamide 1.6 gm, and rifampicin 600 mg. The patient was reviewed after one month. There was no improvement after continuing ATT for one-and-a-half years. On regular follow-up, no side effects of ATT were noted. | Figure 2: MRI brain suggestive of multiple ring-enhancing lesions in the left frontal lobe (a) and right cerebellum (b) and brainstem predominantly in midbrain (c-e)
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 | Figure 3: Chest X-ray showing active infiltrate in the upper lobe of left lung, suggestive of pulmonary tuberculosis
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Discussion | |  |
Tuberculomas are conglomerate, caseating foci that arise within the leptomeninges, ventricles, or the subdural space, though they are usually located within the substance of the brain. They develop during a period of hematogenous dissemination of Mycobacterium tuberculosis and commonly occur in patients who have a history of pulmonary tuberculosis.[2],[3] However, tuberculomas may also become symptomatic in patients with no history of tuberculosis and who have no evidence of pulmonary disease by chest X-ray.[4] In this latter group of patients, neurological symptoms and signs may be the initial manifestation of underlying disseminated tuberculosis.[5] The diagnosis of a tuberculoma is usually ascertained by pathology, neuroimaging, or clinical response to ATT.[6] MRI has revolutionized the imaging of tuberculomas and the diagnosis can be made with certainty to a reasonable extent. The lesions appear hypointense—with or without central hyperintensity (due to caseous necrosis)—or isointense that enhance after intravenous injection of contrast and are associated with significant surrounding brain edema.[7] MRS adds excellent value in the specific diagnosis of tuberculoma in the case of ring-enhancing lesions, wherein it demonstrates a very high lipid peak, reduction in NAA, creatinine, and a choline-to-creatinine ratio of >1. The differential diagnosis based on radiological findings includes cysticercosis, malignant lesions, sarcoidosis, pyogenic abscess, and toxoplasmosis.[8] Our patient had the typical MRI findings of tuberculoma, further confirmed by MRS. Saxena et al. described a case of supranuclear gaze palsy as a manifestation of a tuberculous brain stem lesion.[9] In another report by Monteiro and Coppeto,[10] the patient presented with diplopia and abnormal eye movements and had supranuclear gaze palsy and reduced abduction due to tuberculomas of brain stem and cerebellum.
Conclusion | |  |
To the best of our knowledge, this is the first reported case of bilateral third- and fourth-nerve palsy in a case of brainstem tuberculoma. Most patients respond well to medical therapy and do not require surgical intervention. Delays in diagnosis and treatment result in poor prognoses and severe neurological sequelae. Thus, the prognosis of CNS tuberculoma is related to the timing of initiating appropriate therapy.
In summary, when a patient presents with abrupt onset oculomotor nerve palsy, rapid re-diagnosis should be undertaken and proper treatment initiated because the prognosis is critically dependent on the timing of adequate treatment.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Talamás O, Del Brutto OH, García-Ramos G. Brain-stem tuberculoma. An analysis of 11 patients. Arch Neurol 1989;46:529-35. |
2. | Iraci G, Giordano R, Gerosa M, Pardatscher K, Tomazzoli L. Tuberculoma of the anterior optic pathways. Case report. J Neurosurg 1980;52:129-33. |
3. | Bishburg E, Sunderam G, Reichman LB, Kapila R. Central nervous system tuberculosis with the acquired immunodeficiency syndrome and its related complex. Ann Intern Med 1986;105:210-3. |
4. | Braumann D, Reschofsky K, Mainzer K, Müller-Jensen A. [The manifestations of extrapulmonary tuberculosis]. Dtsch Med Wochenschr 1946 1991;116:611-6. |
5. | Shen WC, Cheng TY, Lee SK, Ho YJ, Lee KR. Disseminated tuberculomas in spinal cord and brain demonstrated by MRI with gadolinium-DTPA. Neuroradiology 1993;35:213-5. |
6. | Fitz CR. Inflammatory diseases of the brain in childhood. AJNR Am J Neuroradiol 1992;13:551-67. |
7. | Berthier M, Sierra J, Leiguarda R. Intraventricular tuberculoma. Neuroradiology 1987;29:163-7. |
8. | Seth R, Kalra V, Sharma U, Jagannathan N. Magnetic resonance spectroscopy in ring enhancing lesions. Indian Pediatr 2010;47:803-4. |
9. | Saxena R, Menon V, Sinha A, Sharma P, Kumar DA, Sethi H. Pontine tuberculoma presenting with horizontal gaze palsy. J Neuroophthalmol 2006;26:276-8. |
10. | Monteiro ML, Coppeto JR. Cryptic disseminated tuberculosis presenting as gaze palsy. J Clin Neuroophthalmol 1985;5:27-9. |
[Figure 1], [Figure 2], [Figure 3]
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