Studded Brainstem Tuberculoma Presenting with Bilateral Inter-Nuclear Ophthalmoplegia.

Abstract

Sir, A 17-year-old male with a history of low-grade fever for 2 months, headache for 15 days, and diplopia and drooping of the right upper eyelid for 10 days, was admitted to our hospital. There was no history of altered sensorium, convulsion, weakness, paresthesia, weight loss, or cough. There was no history of trauma, joint pain, rash, and high-risk behavior. His general examination was normal. Nervous system examination revealed a Glasgow Coma Scale of 15, normal visual acuity with bilateral Grade 2 papilledema, bilateral restriction of adduction movement of the eyeball with ptosis of the right eye, and dilated fixed right pupil [Figure 1a]. The rest of cranial nerve examination was unremarkable. He had bilateral upper motor neuron quadriparesis with power of 4+/5 with bilateral extensor plantars. Sensory and cerebellar functions were intact. Meningeal signs were present. Rest of the systemic examination was unremarkable.Figure 1: (a) On presentation, clinical image showing right-sided ptosis with restriction of bilateral adduction. MRI brain (i-iv) showing multiple T2 hypointense/FLAIR hyperintense signal changes in midbrain with ring enhancement in gadolinium contrast along with hydrocephalus. (b) At 1 month of follow-up, clinical image showing improvement in right-sided ptosis with reduced restriction of bilateral adduction. MRI brain (i-iv) showing reduction of midbrain lesions and resolving hydrocephalus. MRI: Magnetic resonance imaging, FLAIR: Fluid-attenuated inversion recoveryHis laboratory blood parameters showed normal hemogram with normal renal, liver, and thyroid functions with normal glucose and electrolytes. Serological examination was negative for HIV, hepatitis B and C, Leptospira, and Listeria. His cerebrospinal fluid examination revealed lymphocytic pleocytosis with elevated protein level, CBNAAT negative state, negative for Gram stain, fungal stain, and culture sensitivity. Magnetic resonance imaging (MRI) brain revealed multiple coalesced ring enhancing lesions of the midbrain with extension to upper pons with hydrocephalus [Figure 1a]. He was started on standard antitubercular treatment and corticosteroid. He showed improvement clinically within 10 days in the form of partial recovery in ptosis and adduction movements of the eyeball [Figure 1b]. Headache and fever resolved within 2 weeks. MRI brain was repeated at 1 month, which showed resolving hydrocephalus and reduction in size of the brainstem tuberculomas [Figure 1b]. The entity of the brainstem tuberculoma is a rare phenomenon in tuberculosis of central nervous system with incidence of 2.5%–8%.[1] The clinical presentation of the brainstem tuberculoma is pleomorphic. The site, size, and morphology of the lesions determine this versatility of manifestation.[2] Nuclear gaze palsy, ocular motor palsy, facial palsy, bulbar palsy, ataxia, and long tract signs are some important features of brainstem involvement.[3] A multitude of etiology can have similar presentation of brainstem encephalitis including infections, autoimmune disorders, neoplastic (gliomas), and vascular. Brainstem lesions are notorious for complications in the form of hydrocephalus, respiratory insufficiency, fatal arrhythmias, and brain herniation.[4] A thorough workup and aggressive management is prudent for correct diagnosis and better outcome. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.