ISSN - 0973-0958

Isolated Demyelinating Optic Neuritis in Neurotuberculosis

01/09/2014 00:00:00 https://www.pediatriconcall.com/Journal/images/journal_cover.jpg
   
 

Isolated Demyelinating Optic Neuritis in Neurotuberculosis

Souvik Mitra, Moumita Samanta, Mihir Sarkar, Sukanta Chatterjee.
Department of Pediatrics, Medical College, Kolkata, India.
Cite this article  Copy Citation
Mitra S, Samanta M, Sarkar M, Chatterjee S. Isolated Demyelinating Optic Neuritis in Neurotuberculosis. Pediatr Oncall J. 2010;7: 46-47.

Address for Correspondence
Souvik Mitra, 618, Block "O", New Alipore, Kolkata - 700 053, West Bengal, India.
 
Email
souvik4sphs@yahoo.com
 
Abstract
Isolated demyelinating optic neuritis is a rare presenting feature of neurotuberculosis in the pediatric population. Most of the optic neuritis cases that are reported in pediatric tuberculosis are usually associated with other focal neurodeficits or follow anti-tubercular therapy, especially ethambutol. Here we report a 9 year old boy presenting with fever, headache and rapid onset blindness with no focal neurodeficits. He was diagnosed with demyelinating optic neuritis with evidence of neurotuberculosis and was managed successfully with anti-tubercular drug therapy and corticosteroids. Being an endemic country, neurotuberculosis should be considered as a potential cause of demyelinating optic neuritis in the pediatric population.
 
Keywords
Isolated optic neuritis, neurotuberculosis, demyelination
 
Introduction
Neurotuberculosis is a very common but equally serious form of tuberculosis affecting the pediatric population of India. It accounts for up to 10% of all cases of pediatric tuberculosis in this country (1). Isolated optic nerve lesion with rapid onset blindness in a case of neurotuberculosis is rarely reported in the pediatric population.
 
Case Report
A nine year old boy presented with a history of low grade fever for 14 days associated with intense headache and pain on moving the eyes followed by rapid onset blindness affecting both eyes. There was no associated convulsions, altered sensorium, neurodeficits, bladder or bowel dysfunction. There was also no history of head injury, drug intake or any similar complaints in the past. There was no similar history in any of the family members but the child had multiple positive history of contact with tuberculosis. Both his father and paternal grandfather had been on anti-tubercular drugs (ATD) in the past one and half years.

On examination the child was conscious and oriented. There were no focal neurodeficits. On ocular examination, perception of light (PL) was present but projection of rays (PR) was absent. Pupils were bilaterally dilated, sluggishly reacting and there was evidence of relative afferent pupillary defect. Field of vision and colour vision could not be tested due to poor visual acuity. Direct ophthalmoscopy revealed diffuse hyperemia and edema of the optic disc in both the eyes with a normal macula and retina, suggestive of bilateral papillitis. There was no evidence of any other cranial nerve involvement. Other systems were within normal limits. On anthropometric examination his height was 127cm and weight was 19kgs.

Baseline hematological investigations revealed anemia (Hemoglobin 9.5 gm %) with a moderately raised ESR (65mm in the first hour). Cerebrospinal fluid (CSF) analysis revealed a normal cell count (5 cells; all lymphocytes), normal sugar (67mg% with a corresponding blood sugar of 78 mg %) and raised protein (103 mg %). Mantoux test was positive (+10mm). Chest X Ray was normal. No acid-fast bacilli were found on Zeihl-Neilsen staining and microscopy of 3 consecutive gastric aspirates. CT scan brain was normal. MRI brain revealed bilaterally swollen optic nerves and diffuse high signal intensities in the region of the optic nerves and optic chiasma on T2 weighted images suggestive of optic neuritis. (Fig. 1) Visual Evoked Potential (VEP) showed bilateral demyelination of the optic nerves. CSF study for oligoclonal bands was negative. DNA Polymerase Chain Reaction (PCR) study for Mycobacterium tuberculosis antigen from the CSF was positive.

Fig 1. MRI brain showing bilaterally swollen optic nerves with high signal intensities in the region of the optic nerves and optic chiasma


Hence the patient was put on DOTS (Directly Observed Treatment, Short Course) therapy with a four drug anti-tubercular regime (Isoniazid, Rifampicin, Pyrazinamide, Streptomycin) on alternate days for the initial 2 months followed by Isoniazid and Rifampicin on alternate days for the next 4 months according Category 1 of the Revised National Tuberculosis Control Programme (RNTCP) guidelines. The patient was simultaneously put on a 3 day course of pulse Methylprednisolone (at 30mg/kg/day) followed by oral prednisolone (at 2mg/kg/day) in 3 divided doses for 6 weeks with slow tapering over the next 2 weeks.

Ocular examination at the end of the second week of therapy revealed a normal PL and PR, slightly dilated pupils with normal direct and consensual light reflex in both the eyes. Vision was 6/60 bilaterally without any apparent field defects or dyschromatopsia. The hyperemia and edema of the optic disc had also resolved. At the end of 3 months the child had gained weight appreciably (22.5 kgs), vision was 6/12 in both eyes and CSF study was negative for M. tuberculosis by DNA PCR method. After 6 months of ATD, MRI brain revealed a normal study, visual acuity was 6/6 in both the eyes with a normal color vision and field of vision.
 
Discussion
Loss of vision is a well documented sequelae of neurotuberculosis. The tubercle bacilli may cause loss of vision by affecting the central nervous system (CNS) directly. This occurs in cases of involvement of the optic nerve and optic chiasma by tuberculomas, in miliary tuberculosis and optochiasmatic arachnoiditis (2,3). But the bacilli may also affect the CNS by producing a hypersensitivity reaction to the tuberculoprotein leading to "allergic tuberculous encephalopathy". This hypersensitivity reaction may induce perivascular demyelination of white matter and may present with optic neuritis (4). Similar cases have been reported in the adult population by Balal et al and Stechschulte et al where the presenting feature of tuberculosis was isolated optic neuritis which responded dramatically to ATD with corticosteroids (5,6). But little is known about similar presentations in the pediatric population.

Optic neuritis in pediatric population is mostly due to demyelinating diseases like acute demyelinating encephalomyelitis, multiple sclerosis and Devic's disease (neuromyelitis optica). Optic neuritis has been known to occur with the use of Ethambutol and hence was avoided in our patient (7). Therapy includes a pulse therapy of methylprednisolone for 3 days followed by oral prednisolone for 11 days (8). But in view of definitive evidence of neurotuberculosis in our case by positive DNA PCR study in CSF, prednisolone was continued for 8 weeks along with ATD with promising results.

Thus, in an endemic country like India, where tuberculosis presents with various forms of clinical manifestations, neurotuberculosis should always be ruled out in a child presenting with sudden onset of blindness.

Contributors: S Mitra and M Samanta were involved in the diagnosis and management of the case. S Mitra drafted the article with help of M Sarkar. S Chatterjee critically evaluated the manuscript.
 
Funding
None
 
Conflict of Interest
None
 
References :
  1. Gulati S, Kalra V, Seth R, Seth V. Neurotuberculosis - Clinical manifestations, diagnosis and Management. In: Seth V, Kabra SK (eds). Essentials of Tuberculosis in Children. 3rd Edn. Jaypee. New Delhi. 2006; 157- 228.  [CrossRef]
  2. Kadioglu HH, Gundogdu C, Deniz O, Takci E, Tuzun Y, Aydin IH. Optochiasmatic tuberculoma-case report and review. Zentralbl Neurochir. 1996; 57: 30-36.  [PubMed]
  3. Scott RM, Sonntag VK, Wilcox LM, Adelman LS, Rockel TH. Visual loss from optochiasmatic arachnoiditis after tuberculous meningitis. Case report. J Neurosurg. 1977; 46: 524-526.  [CrossRef]
  4. Dastur DK, Manghani DK, Udani PM. Pathology and pathogenetic mechanisms in neurotuberculosis. Radiol Clin North Am. 1995; 33: 733-752.  [PubMed]
  5. Stechschulte SU, Kim RY, Cunningham ET Jr. Tuberculous neuroretinitis. J Neuroophthalmol. 1999; 19: 201-204.  [CrossRef]
  6. Balal M, Paydas S, Seyrek N, Karayaylali I. Loss of vision and renal function in a patient with miliary tuberculosis. Mt Sinai J Med. 2005; 72: 124-126.  [PubMed]
  7. Filipovic T, Bujanic-Cuculic S, Boskovic I. Optic nerve damage caused by administration of ethambutol. Lijec Vjesn. 1997; 119: 273-274.  [PubMed]
  8. Kanski JJ. Neuro-ophthalmology. In: Kanski, JJ ed. Clinical Ophthalmology. A Systemic Approach. 3rd ed. Oxford, England: Butterworth-Heinemann Ltd. 1994: 601-603.

Last Updated : 01 June 2010 Vol 7 Issue 6 Art #32

Cite this article as: :
Mitra S, Samanta M, Sarkar M, Chatterjee S. Isolated Demyelinating Optic Neuritis in Neurotuberculosis. Pediatr Oncall J. 2010;7: 46-47.
ask a doctor
Ask a Doctor
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License
Disclaimer: The information given by www.pediatriconcall.com is provided by medical and paramedical & Health providers voluntarily for display & is meant only for informational purpose. The site does not guarantee the accuracy or authenticity of the information. Use of any information is solely at the user's own risk. The appearance of advertisement or product information in the various section in the website does not constitute an endorsement or approval by Pediatric Oncall of the quality or value of the said product or of claims made by its manufacturer.
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0