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CASE REPORT
Year : 2021  |  Volume : 10  |  Issue : 3  |  Page : 205-208

Abducens nerve palsy: A sole presentation of isolated cerebellar tuberculoma


Department of General Medicine, Government Medical College and Hospital, Chandigarh, India

Date of Submission31-Aug-2021
Date of Decision11-Oct-2021
Date of Acceptance12-Oct-2021
Date of Web Publication17-Mar-2022

Correspondence Address:
Dr. Gautam Jesrani
Department of General Medicine, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdrntruhs.jdrntruhs_120_21

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  Abstract 


Tuberculomas constitute 5–30% of the space-occupying lesions of the central nervous system (CNS) in developing countries, and children and young adults are the most affected population. Most CNS tuberculomas include focal neurological signs with evidence of either meningeal exudates or hydrocephalus, but presentation as isolated sixth nerve palsy is very rare. We report a case of an immunocompetent female who presented with double vision, and was found to have isolated abducens nerve palsy of the right eye. On magnetic resonance imaging of the brain, solitary cerebellar tuberculoma was identified without any evidence of meningitis, basal exudate, or hydrocephalus. Despite the prompt initiation of anti-tubercular drugs and steroids, negligible improvement was noticed at 2 weeks of follow-up. This report highlights that isolated tuberculoma of any unrelated brain region can cause lateral rectus palsy, which may result in permanent disability.

Keywords: Abducens nerve, cerebellar tuberculoma, concealed meningitis, false localizing sign, magnetic resonance imaging, mycobacterium tuberculosis


How to cite this article:
Gupta S, Arora S, Gupta S, Jesrani G, Gupta M. Abducens nerve palsy: A sole presentation of isolated cerebellar tuberculoma. J NTR Univ Health Sci 2021;10:205-8

How to cite this URL:
Gupta S, Arora S, Gupta S, Jesrani G, Gupta M. Abducens nerve palsy: A sole presentation of isolated cerebellar tuberculoma. J NTR Univ Health Sci [serial online] 2021 [cited 2022 Nov 30];10:205-8. Available from: https://www.jdrntruhs.org/text.asp?2021/10/3/205/339798




  Introduction Top


Tuberculosis (TB) is among the oldest and most lethal infectious diseases worldwide, with increased prevalence in developing countries. No country has a higher TB burden than India, which accounts for a quarter of the 10 million global TB cases and 1.4 million TB deaths each year.[1] The central nervous system (CNS) TB constitutes only 1% of the total TB cases, yet represents the most severe form of the disease, conferring the highest rates of morbidity and mortality. The most common presentation of CNS TB is tuberculous meningitis, and other manifestations include intracranial tuberculoma, cerebral abscess, meningoencephalitis, arteritis, Pott's paraplegia, and arachnoiditis.[2] CNS tuberculoma is a localized metastatic tubercular activity, which occurs simultaneously with underlying meningitis customarily. Focal neurological deficit is the most common clinical appearance, pertaining to the site of tuberculoma but presentation as the isolated sixth nerve palsy in the absence of meningitis or hydrocephalus is very rare.[3]


  Case Presentation Top


A 12-year-old girl with no previous morbidities was referred to our tertiary health center with horizontal gaze paralysis of the right eye from the last 6 h. The patient also had a complaint of diplopia on looking to the right lateral side, which started with ocular paralysis, and there was no preceding history of nausea or vomiting, neck stiffness, and trauma. No other complaints like headache, ear discharge, or previous eye infection were experienced, and she had normal development, according to her parents. Also, the patient was immunized to date as per the national immunization schedule.

On presentation, the patient had invariably stable vitals including blood pressure, temperature, and blood glucose. On systemic examination, she had normal cardiovascular and respiratory system findings. The nervous system examination revealed no neck rigidity and a flexor plantar response bilaterally. Also, she did not demonstrate gait abnormality or any cerebellar sign. The ocular examination depicted restricted lateral movement of the right eye [Figure 1], without any other gaze restriction, nystagmus, and pupillary abnormality in both the eyes. There were no signs of local inflammation or ocular tenderness. Her fundus examination demonstrated a normal optic disk and vessels in both eyes, and the other cranial nerve evaluation was inconclusive.
Figure 1: (a) Right lateral gaze palsy as the right eye is unable to move toward the right side. (b) Normal left lateral gaze in both

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The blood investigation revealed normal hemoglobin, leukocyte count, liver function tests, and urine analysis. The chest X-ray was normal and the electrocardiogram had a normal conduction activity. Her visual acuity was 6/6 on the left side and 6/9 on the right side. She was advised for eye patching on the affected side initially to alleviate diplopia. In the absence of any ocular cause for the right lateral palsy, she was subjected to contrast-enhanced magnetic resonance imaging (MRI) of the brain. The imaging study depicted normal meninges, optic nerve, and the frontal, parietal, and occipital lobes [Figure 2]a and [Figure 2]b. Surprisingly, the right cerebellar hemisphere had a round, well-defined lesion of 7.6 mm × 6.7 mm on fluid-attenuated inversion recovery (FLAIR) and T1-weighted images [Figure 2]c and [Figure 2]d. So, the possibilities of tuberculoma and neuro-cysticercosis (NCC) were kept. Further, she was subjected to cerebrospinal fluid (CSF) analysis, which was acellular with a protein of 68 mg/dL (normal 15–45), glucose of 47 mg/dL (normal 50–75), and adenosine deaminase (ADA) levels of 12 U/L normal <10). Acid-fast bacilli staining was negative in CSF and the culture had no organism growth. Moreover, the cysticercosis antibody levels in the CSF by enzyme-linked immunoassay were within the normal range, but the cartridge-based nucleic acid amplification test (CBNAAT) for TB had a positive result. Thus, the diagnosis of cerebellar tuberculoma was established on the basis of the CBNAAT test, mildly raised ADA levels, and negative serology for NCC. She was started on standard weight-based anti-tubercular treatment (ATT), i.e., isoniazid (5 mg/kg), rifampicin (10 mg/kg), ethambutol (15 mg/kg), and pyrazinamide (25 mg/kg) on the 4th day of hospital admission. Along with this, steroids (dexamethasone 0.4 mg/kg in divided doses) and pyridoxine were also instituted. A follow-up after 2 weeks demonstrated negligible improvement in the ocular weakness, so the patient was advised for corrective surgeries but denied any intervention. Her morbidity persisted even after 3 months of the recommended treatment and regular follow-up.
Figure 2: Magnetic resonance imaging of the brain (contrast-enhanced T1-weighted) demonstrating no meningeal enhancement, basal exudate, or hydrocephalus (a) coronal section, (b) axial section. Solitary ring-enhancing right cerebellar lesion on magnetic resonance imaging suggestive of tuberculoma (c) fluid-attenuated inversion recovery [FLAIR] and (d)contrast-enhanced T1-weighted images

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  Discussion Top


Tuberculomas are conglomerate caseating foci that arise within the leptomeninges, ventricles, or the subdural space, though usually located within the brain parenchyma. They develop during a period of hematogenous dissemination of Mycobacterium TB and commonly occur in patients who have a history of pulmonary TB, tuberculous, meningitis, or both.[4] However, tuberculomas may be encountered in patients with no current or previous history of TB, and among these, neurological symptoms and signs may be the initial manifestation of the underlying disseminated disease.[5]

The diagnosis of intracranial tuberculoma is usually ascertained by neuroimaging characteristics [Table 1], CSF CBNAAT test, and clinical response to ATT in some cases.[6] CSF evaluation for routine parameters can also rule out other potential differentials, apart from TB confirmation with relatively specific investigations like ADA and Gene-Xpert or CBNAAT. MRI has revolutionized the imaging of tuberculomas, and the diagnosis can be made with certainty to a reasonable extent. The lesions may appear hypointense, with or without central hyperintensity (due to caseous necrosis), or isointense, which can enhance after intravenous injection of the contrast. These lesions are commonly associated with significant surrounding parenchymal edema and can virtually affect any intracranial structure.[5] Magnetic resonance spectroscopy (MRS) is a relatively newer modality, which can be applied during an MRI scan and demonstrates a characteristic lipid-lactate peak around the tubercular lesion.
Table 1: Radiographic Features of Central Nervous System Tuberculomas

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Tubercular meningitis and associated hydrocephalus usually present with various false localizing signs, and the sixth nerve palsy, either unilateral or bilateral, is one classic example among these. It occurs in the context of raised intracranial pressure of whatever cause and is considered as the most common of the false localizing signs.[7] The pathophysiological process of the sixth nerve palsy with increased intracranial pressure has traditionally been said to be the stretching of the nerve in its long intracranial course or compression against the petrous ligament or the ridge of the petrous temporal bone. In our case, concealed meningitis or ongoing inflammation could be the possible mechanism for abducens nerve palsy, which was identified by CBNAAT and mildly raised ADA.

If the clinical suspicion is high and the patient belongs to the endemic zone, ATT should be initiated, even in the absence of confirmatory test results. Combination therapy, initially consisting of a four-drug regime, i.e., isoniazid (H), rifampicin (R), pyrazinamide (Z), and ethambutol (E), reduces the likelihood of developing drug resistance and enhances the combined bactericidal effect. The national guidelines of India for the treatment of intracranial TB recommend standard first-line ATT for at least 9 months (HRZE), followed by HRE or HRZ therapy for a minimum of 7 months, and adjuvant corticosteroid drugs for at least 4 weeks.[8] Pyridoxine, 25 mg daily, should be added to all anti-tubercular regimens to prevent isoniazid-induced peripheral neuropathy. Adjunctive corticosteroid therapy is recommended for all patients with CNS TB as it limits tissue damage by reducing inflammation.[4] Also, steroids increase the rate of resolution of basal exudates and tuberculomas, leading to improved survival. A delay in the diagnosis establishment or treatment initiation can lead to different complications like hydrocephalus and cerebral abscess, and surgical procedures like shunt procedure or craniotomy may be necessary for the definitive management.


  Conclusion Top


The sixth cranial nerve has a long intracranial course and can be affected anywhere along its pathway; therefore, etiological diagnosis of this nerve palsy demands extensive investigations. Intracranial tuberculoma of any location can lead to concealed meningitis and should be considered in patients with any cranial nerve palsy, especially for the sixth cranial nerve palsy. Cerebellar tuberculoma presenting as isolated abducens nerve involvement is rarely outlined and customarily reported cases have concurrent hydrocephalus or basal exudates, but these changes may be absent, as observed in our case. Further, prompt initiation of ATT, along with steroids and pyridoxine, is crucial in the early disease stages to prevent disability, but permanent afflictions are not uncommon.

Declaration of patient consent

A written consent is present, duly signed by the parents of the patient. The authors obtained the consent after explaining that no identity will be revealed and the case information, including pictures will be used for education purpose only. They were also explained that the journal publication will not contain any material or picture, disclosing patient's identity. The parents of the patient gave positive consent for publication and authors certify that written consent is present, procured for publication.

Ethical approval

A proper written consent is present, which was obtained from the parents of the patient, for the use of the data related to this case.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
WHO: Global tuberculosis report 2020. Available from: https://www.who.int/publications/i/item/9789240013131. [Last accessed on 2021 Aug 24].  Back to cited text no. 1
    
2.
Changal KH, Raina AH. Central nervous system manifestations of tuberculosis: A review article. J Mycobac Dis 2014;4:146-50.  Back to cited text no. 2
    
3.
Zia-Ul-Hussnain HM, Farrell M, Looby S, Tormey W, Javadpour M, Mcconkey S, et al. Pituitary tuberculoma: A rare cause of sellar mass. Ir J Med Sci 2018;187:461-4.  Back to cited text no. 3
    
4.
Schaller MA, Wicke F, Foerch C, Weidauer S. Central nervous system tuberculosis: Etiology, clinical manifestations and neuroradiological features. Clin Neuroradiol 2019;29:3-18.  Back to cited text no. 4
    
5.
Kowsalya A, Gajarlewar U, Adulkar NG, Kumar SM. Unique case of midbrain tuberculoma presenting as isolated inferior rectus palsy with nystagmus. Indian J Ophthalmol 2018;66:599-602.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Trivedi R, Saksena S, Gupta RK. Magnetic resonance imaging in central nervous system tuberculosis. Indian J Radiol Imaging 2009;19:256-65.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Larner AJ. False localizing signs. J Neurol Neurosurg Psychiatry 2003;74:415-8.  Back to cited text no. 7
    
8.
Sharma SK, Ryan H, Khaparde S, Sachdeva KS, Singh AD, Mohan A, et al. Index-TB guidelines: Guidelines on extrapulmonary tuberculosis for India. Indian J Med Res 2017;145:448-63.  Back to cited text no. 8
[PUBMED]  [Full text]  


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