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 Table of Contents  
CASE SERIES
Year : 2022  |  Volume : 34  |  Issue : 1  |  Page : 51-54

Neuro-ophthalmic manifestations of central nervous system tuberculosis: Compilation of three diverse unique presentations


1 Assistant Professor, Department of Ophthalmology, Dr. D. Y. Patil Medical College, Nerul, Navi Mumbai, Maharashtra, India
2 Resident Ophthalmology, Dr. D Y Patil Medical College, Navi Mumbai, Maharashtra, India
3 Department of Ophthalmology, Dr. D Y Patil Medical College, Navi Mumbai, Maharashtra, India

Date of Submission18-Dec-2020
Date of Acceptance04-Jan-2021
Date of Web Publication21-Apr-2022

Correspondence Address:
Dr. Harsha Sammer Pagad
Dr. D. Y. Patil Medical College and Hospital and Research Centre, Sector 5, Nerul, Navi Mumbai - 400 706, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kjo.kjo_205_20

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  Abstract 


Tubercular meningitis is the most devastating form of tuberculosis. Neuro-ophthalmic involvement can manifest as cranial nerve palsies, pupil abnormalities, disc changes, like papillitis, papilloedema, or optic atrophy and choroidal tubercles. The rate and extent of recovery are strongly. Related to early diagnosis and treatment. Herein, we describe a constellation of three cases of central nervous system tuberculosis with aberrant regeneration of oculomotor nerve, optochiasmatic arachnoiditis presenting as bilateral primary optic atrophy and the last case of parietal lobe tuberculoma presenting as homonymous hemianopia, each one with its own characteristic ocular findings.

Keywords: Central nervous system tuberculosis, neuro-ophthalmic manifestations, rare


How to cite this article:
Pagad HS, Hariyani R, Jain A, Shanbhag N. Neuro-ophthalmic manifestations of central nervous system tuberculosis: Compilation of three diverse unique presentations. Kerala J Ophthalmol 2022;34:51-4

How to cite this URL:
Pagad HS, Hariyani R, Jain A, Shanbhag N. Neuro-ophthalmic manifestations of central nervous system tuberculosis: Compilation of three diverse unique presentations. Kerala J Ophthalmol [serial online] 2022 [cited 2022 May 16];34:51-4. Available from: http://www.kjophthal.com/text.asp?2022/34/1/51/343675




  Introduction Top


Tuberculosis is one of the commonest ailments in India and the neuro ophthalmic manifestations are quite devastating leading to permanent loss of vision in young adults. The various presentations are nerve palsies, optic atrophy, papillitis etc.


  Case Reports Top


The first case is of a 15 years old female fever, headache, vomiting, tinnitus, seizures for the past 3 months with history of gradual painless decrease in vision with sudden onset binocular horizontal diplopia. The best corrected visuals acuity was counting fingers at 1 m in right eye and counting finger at one and half meter in the left eye. Pupillary evaluation showed sluggishly reacting pupils in both eyes with relative afferent pupillary defect (RAPD) in the right eye. There was −1 limitation of abduction in both eyes. On alternate cover test there was alternating esotropia which measured 30 prism diopters for distance and 16 prism diopters for near. Dilated fundus examination showed temporal pallor in both eyes [Figure 1]. Cerebrospinal fluid examination showed lymphocytosis with elevated proteins. Magnetic resonance imaging (MRI) revealed shaggy meningeal enhancement in right frontotemporal region, right perisylvian cistern, and right half of surpasellar cistern [Figure 2] suggestive of optochiasmatic arachnoiditis accounting for asymmetric decreased vision and RAPD in the right eye. The patient was started on anti-tubercular therapy and steroids. At 2 months' follow-up, the visual acuity remained same but with resolution of diplopia. Optochiasmatic arachnoiditis remains one of the potential causes of primary optic atrophy with permanent loss of vision in tubercular meningitis (TBM).
Figure 1: Colour Fundus photograph showing bilateral primary optic atrophy (a) left eye (b) right eye

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Figure 2: Magnetic resonance imaging: (a) Enhancement in right frontotemporal region, (b) right perisylvian cistern, and (c) right half of suprasellar cistern

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The second case is of a 15-year-old girl presented to ophthalmology outpatient department with a history of the left eye remaining open when looking down since the past 8 months. She also complained of binocular horizontal diplopia in up and down gaze. She was diagnosed with TBM (for her symptoms of fever, headache, vomiting, backache, lower limb paresthesia with a history of inability to walk, seizures) with cerebellar involvement with left eye pupil involving complete third nerve palsy 8 months ago. She was receiving anti-tubercular therapy (Category 2) for a year. Contrast enhanced computed tomography scan at that time showed Few disc and ring T2 hypo-intense enhancing lesions with surrounding vasculogenic edema in the right parietal post central cortex, bilateral cerebellar hemisphere, and inferior vermis with subtle blooming on Gradient echo sequences (GRE) seen in inferior vermis lesion possibly calcification suggestive of infective etiology and an acute nonhemorrhagic infarct most likely vasculitis in pontine region [Figure 3].
Figure 3: (a,b) CECT scan showing few disc and ring T2 hypo intense lesions in right parietal cortex and calcification in bilateral cerebellar hemisphere, (c) Acute non haemorrhagic infarct in pons

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On examination, her unaided visual acuity recorded 20/20, N6 in both eyes. Ocular motility examination was normal in right eye. Color vision testing with Ishihara chart was normal in both eyes. Extraocular motility evaluation revealed −3 limitation of elevation and −2 limitation of depression in left eye. Signs of aberrant regeneration such as Pseudo von Graefe's Signs, Pseudo Duane's Sign were present. Pupil in the left eye was mid-dilated sluggish reaction to light. Pupillary constriction was noted and measured with a pupil scale when eye adducted and converged, i.e., pseudo Argyll Robertson sign present [Figure 4]. Fundus examination was unremarkable in both eyes.
Figure 4: Signs of aberrant regeneration

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We report third case of homonymous hemianopia due to presumptive cerebral tubercular granulomas in a young adult as one of the neuro-ophthalmic presentation of central nervous system (CNS) tuberculosis.

A 19-year-old female presented with acute onset headache, binocular diplopia, blurry vision. Her best-corrected visual acuity was 6/12 p in both eyes with sluggishly reacting pupils in both eyes. Color vision recorded with Ishihara's pseudoisochromatic chart was 11/16 in right eye and 7/16 in left eye. There was-1/2 limitation of abduction in both eyes. She had alternating esotropia on alternate cover test which measured 25 prism diopter for distance and near 14 prism diopter suggestive of bilateral sixth nerve paresis. Automated perimetry detected incongruous left homonymous hemianopia [Figure 5]. On dilated fundus examination, the patient had grade 2 papilledema [Figure 6].
Figure 5: Left-sided homonymous hemianopia, 30-2 field of (a) left eye (b) right eye

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Figure 6: Papilledema at presentation (a) left eye, (b) right eye and resolution at 2 months follow-up, (c) left eye, (d) right eye

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A MRI study was ordered in view of above findings. MRI of brain/orbit showed The presence of right parieto-occipital tuberculomas [Figure 7]. She was mantoux positive the patient was started on AKT along with steroids and mannitol at 2 months' follow, the patient had resolution of papilledema and sixth nerve paresis with recovery of vision.
Figure 7: MRI Brain: Right parieto-occipital granulomas, (a) coronal, (b)transverse

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  Discussion Top


TB is still a very common ailment in India. The most serious form of tuberculosis is TBM.[1] Tuberculomas account for 5%–30% of intracranial space occupying lesions often affecting children and young adults and TBM can have different ocular involvement in the form of choroidal tubercles, papillitis, optic atrophy, and nerve palsies.[2] There have been multiple publications quoting the incident of various ocular complications in TBM. Verma et al.[3] observed that 76% of children with TBM had ocular findings with third and sixth cranial nerves being frequently involved. In another study by Lamba et al.[4] of 48 children with TBM, optic disc changes (papillitis) constituted 62%, pupillary involvement was in 48% of patients and cranial nerves (3rd) involvement was found in 28% of patients. Anupriya et al.[5] observed that optochiasmatic arachnoiditis can occur as a complication of TBM.

Vision impairment is one of the most devastating sequelae associated with CNS TB causing significant morbidity. Vision impairment may result from optochiasmati arachnoiditis, compression of optic nerve by tuberculoma, optic nerve granuloma, optic neuritis associated with anti-tubercular therapy, vasculitic infarcts, or occlusion of arteries supplying the optic nerve by basal exudates.

TBM affects mainly the basal parts of the brain. Exudates present in the interpeduncular, suprasellar and Sylvian cisterns, result in optochiasmatic arachnoiditis and tuberculoma. Optochiasmatic arachnoiditis and tuberculoma are associated with profound vision loss.[6] They are the devastating forms of TBM affecting young adults. There can be enhancing lesions on MRI in the interpeduncular fossa, pontine cistern, and the perimesencephalic and suprasellar cisterns. The management of tuberculous optochiasmatic arachnoiditis and optochiasmatic arachnoiditis tuberculoma has been challenge with usually unsatisfactory outcomes. Corticosteroids such as dexamethasone, methyl prednisolone, thalidomide, and hyaluronidase have been used with variable success. Neurosurgery may be needed in unresponsive cases.[7] Our patient also did not have any improvement in vision despite appropriate treatment.

The second case is of aberrant regeneration of third nerve noted in a case of tubercular meningits with vasculitic infarct in pons. Aberrant regeneration is a very common phenomenon observed with diseases of the third nerve. According to Seddon's classification,[6] aberrancy does not occur in first- and second-degree nerve injuries. It is more common in third degree or neurotmesis where the endoneurium is disrupted. Microvascular ischemic damage to the oculomotor nerve due to small vessel disease as in diabetes rarely is responsible for synkinesis, but there are few case reports following the same.[8] Walsh has reported cases of aberrant regeneration following ischemic insult.[8]

Atypical ophthalmic manifestations may be the initial presenting feature in patients with CNS tuberculosis. This case highlights the need for increased index of suspicion for intracranial tuberculosis in young patients with atypical ophthalmic manifestations in a country like India with wide prevalence of tuberculosis. The perimetry findings correlated with the location of granulomas affection the right optic radiation whereas in cases of papilledema, we expect an enlarged blind spot.

A similar case of homonymous hemianopia as an isolated presentation of tubercular abscess has been reported by Gharai et al.,[9] in a patient with HIV infection.

This case emphasizes the importance of neuroimaging in cases of unusual visual field defects like hemianopia in patients with papilledema to reach an etiological diagnosis like CNS tuberculosis which can be potentially blinding and lethal if left untreated.


  Conclusion Top


TBM can cause irreversible loss of vision and cause a panorama of ocular motor abnormalities. Early timely intervention by a multidisciplinary team of neurologist, ophthalmologist can save eye/vision and life.

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 initial s 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 Top

1.
Das U, Gupta VK, Yadav P, Mediratta V, Rewash BB. Tuberculous meningitits with blindness. JAIME 2010;11:61-2.  Back to cited text no. 1
    
2.
Desai HG, Anklesaria ED. Ophthalmological aspects of tuberculous meningitis. J Indian Med Assoc 1967;49:429-32.  Back to cited text no. 2
    
3.
Verma BM, Srivastav SK, Srivastav JR. Ocular manifestation of tubercular meningitis and their prognostic value in children verma BMD. IJO 1981;29:301-2.  Back to cited text no. 3
    
4.
Lamba PA, Bhalla JS, Mullick DN. Ocular manifestations of tubercular meningitis – A clinico-biochemical study. J Pediatr Ophthalmol Strabismus 1986;23:123-5.  Back to cited text no. 4
    
5.
Anupriya A, Sunidhi M, Maya T, Goel M, Alexander M. Tuberculous optochiasmatic arachnoiditis. Neurol India 2010;58:732-5.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Seddon HJ. A classification of nerve injuries. Br Med J 1942:237-9.  Back to cited text no. 6
    
7.
Garg RK, Paliwal V, Malhotra HS. Tuberculous optochiasmatic arachnoiditis: A devastating form of tuberculousmeningitis. Expert Rev Anti Infect Ther 2011;9:719-29.  Back to cited text no. 7
    
8.
Weber E, Newman A. Aberrant regeneration of the oculomotor nerve: Implications for neurosurgeons. Neurosurg Focus 2007;23:E14.  Back to cited text no. 8
    
9.
Gharai S, Venkatesh P, Sinha A, Garg S. Isolated homonymous hemianopsia due to presumptive cerebral tubercular abscess as initial manifestation of human immunodeficiency virus. Indian J Ophthalmol 2012;60:321-4.  Back to cited text no. 9
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

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