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362 AIOC 2009 PROCEEDINGS

TBM (Tubecular Meningitis) is the mostdangerous form of tuberculosis infection and

still the commonest chronic CNS infection indeveloped countries. In adults, it may occur asprimary disease, accounts for 9.1% of extrapulmonary TB cases (Nelson 2004) or secondaryto pulmonary TB. Diverse ocular manifestationsoccur as sequlae of TBM, due to chronicallyraised ICT or retinal vasculitis, in about 70%cases, up to 25% cases show oculocranialpolyneuropathy.1 Ocular manifestation may bethe presenting feature, analyses of which help

AUTHORS’S PROFILE:DR. ANITA MISRA: M.B.B.S and M.S, S.C.B. Medical College, Utkal University, Cuttack,Orissa. LOW VISION training at Aravind Eye Care, Madurai and LVPEI, Hyderabad 2007.Presently, Senior Resident at R.I.O, P.G. Dept. of Ophthalmology, S.C.B. Medical College,Cuttack, Orissa.Email: [email protected]

Neuro-ophthalmic Manifestations of Tubercular Meningitis(TBM) in a Tertiary Eye Care Centre

Dr. Anita Misra, Prof. Madhumati Misra, Prof. Himansu Kumar Rajguru,Dr. Prasant Kumar Nanda

(Presenting Author: Dr. Anita Misra)

detection, diagnosis and monitoring of effects ofmedical Therapy of TBM.

Tuberculous infection usually reaches themeninges by hematogenous route or throughintracranial lymphatic from the cervical nodes.Bacilli are immobilized in end arteries and leadto submeningeal tubercular foci which dischargebacilli into subarachnoid space intermittently,causing perivascular exudation followed bycaseation, gliosis, giant cell proliferation andvaculitis. The major impact falls on basalmeninges (thick exudation surrounds cranial

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363NEURO OPHTHALMOLOGY SESSION

Table-1: Systematic features of TBM patients at presentation (n=60 patients)

Sl. No. Prodromal symptoms Patients(n) Signs of meningitis Patients(n)

1 Fever 38 Altered sensorium 10

2 Cough 26 Neck rigidity 42

3 Anorexia 8 Kernig’s sign 42

4 Weight loss 22 Hypotension 0

5 Vomiting 28 Motor deficit 6

6 Headache 32 Involuntary movement 1

7 Seizure 18 Ocular palsies 23

8 Motor paresis 3 Defective vision 40

Table-2: TBM cases with oculocranial nerve involved at presentation (n=60 patients)

Cranial Commonest Patients(n) II nerve Commonest Patients (n)nerves presentations presentations

II ↓visual function 13 Vision Absent PL 6

<6/18 32

≥6/18 16

III Ptosis 9 Field Scotoma 8

IV — 0 Blind spot enlargement 2

VI Squint 11 ↓ color vision 12

VII Lagophthalmos 4 Fundus Normal 14

Combined Multiple 12 Papilloedema 12

Papillitis 9

Primary OA 7

Secondary OA 18

Table-3: Radiological examination at presentation (n=60 patients)

X-ray chest Enhanced CT

Normal Hilar nodes Miliary Consoli- Normal Hydro- Basal Infarct Tuber-

shadow dation cephalus enhance- culoma

ment

Patient (n) 25 19 9 0 18 32 0 4 6

CSF analysis for TBM was positive in 48 (80%) cases as out lined in Table 4.

Table-4: CSF findings at presentation (n=60 patients)

Examination Patients(n) Examination Patients(n)

Appearance Clear 12 Protein level/mg(%) <100 8

Xanthochromic 20 101-500 32

Cobweb 28 501-1000 12

Cell count/mm3 <50 12 >1000 8

51-100 26 Sugar level/mg(%) <40 38

101-200 12 >40 22

>200 10 AFB stain +ive 4

-ive 56

nerves and major blood vessels at base of brain,basal cisterns, blood vessels (vaculitis, partial orcomplete occlusion, phlebitis) and brainparenchyma (border zone reaction, infarction,tuberculoma).

Classically TBM evolves through 3 stages asdefined by British Council2 as (a) prodromalstage for 2-3 wks, (b) stage of meningeal irritationand (c) stage of cerebral involvement(symptomsof raised intracranial pressure, focal neurological

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deficits , cranial nerve palsies; usually II, III, IV,VI, VII, posterior fossa meningitis, spinalleptomeningitis, lastly coma, decorticatingposture or extensor rigidity with dilated fixedpupils .Papillitis is the commonestneuroophthalmic complication in 60% cases butuveitis and choroid tubercles are rare due to theirdifferent pathogenesis).3

Diagnosis of TBM depends on high index ofclinical suspicion, contact history,immunosuppression,chest X-ray,CT scan/MRI ofbrain and orbit may show nodular enhancinglesion with central hypodensity, central edema,

infarctions, hydrocephalus and multipleintracranial tuberculomas.

CSF analysis and culture is the key to diagnosisof TBM. Faintly visible “spider’s web clot” dueto CSF hyper proteinemia, low sugar withpleocytosis are almost pathognomonic. Acid fastbacilli are seen in CSF in less than 5% cases andculture positive in less than 10%.2,4,5

Dot immunobinding assay (Dot-Iba) forcirculating antimicrobial antibodies in CSF isused for rapid diagnosis.6

Retrospective analysis of the presenting Neuro-

ophthalmic features of diagnosed cases of TBMand correlating with imaging and CSF findings.

Materials and Methods60 proven cases of TBM having neuro-ophthalmic symptoms referred to ourneuro-ophthalmology section from the depts. likeMedicine. Paed. TB/Chest, Neurology,Neurosurgery between July 2005 and Feb 2008were analyzed to describe the demography,Clinical profile, CSF analysis, radiological andimaging study along with detailed neuro-ophthalmic findings. Attempt has been made tocorrelate these manifestations of TBM with eachother.

All patients had received standard ATT andsteroids. Symptomatic treatment given in allpatients included mannitol, antibiotics, IV fluids,antipyretics and physiotherapy.

DiscussionDespite recent advances in Chemotherapy, TBMcaused by typical/atypical mycobacteriumremains a serious medical problem. Clinical andinvestigation procedures may be nonspecific andbacteriological proof difficult to obtain. An

ophthalmologist can assist the neurophysician onreaching a definite diagnosis and in reducingmorbidity and mortality due to TBM by earlyinstitution of appropriate therapy.

In the present study, out of 60 cases, 60% weremale and 40% female.20%were below 20 yrs, 9%were above 60y, maximum cases of 28(46%) in20-40 age group. Highest ocular sequel was seenin 40-60 age group and least complication wereseen in 0-20 years of age. 39(65%) had definitecontact history. Low grade fever was thecommonest presenting symptom in 38(63%).Kerning’ sign of meningeal irritation was thecommonest presenting sign in 42(70%) [Table-1]similar to 81% by Benakappa et.al. 1983.7

Common neuro ophthalmic complications notedwere defective vision in 40(66.6%), diplopia in13(21.6%). Table-2 shows the pattern andincidence of cranial nerve involvement (isolatedand combined) in TBM, which is widely variablein different reported series. The commonestsingle cranial nerve involved was VI nerve in11(18%) cases; combined palsy was thecommonest pattern in 12(20%) cases. Thecommonest pattern of optic nerve involvementwas optic atrophy (POA, SOA) in 25(42%) casespossibly due to late detection of cases, earlierpresentations were papilloedema in 20%,papillitis in 15%, visual field defects in 18%.

Radiological study of chest showed findingssuggestive of pulmonary TB in 35 (54%), mostlyhilar lymphadenopathy in 19(31.6%), but wasnormal in 25(46%) cases suggesting extrapulmonary TBM outlined in Table 3.

Enhanced CT Scan revealed normal result in18(30%), hydrocephalus was commonest findingin 32 (53.3%). Hydrocephalus was reported byOzates et al. (2000)8 in 80% cases. CT evidence of

tuberculomas was noted in 10% cases andinfarction in 6.6% cases, however, Bhargava et.al. (1982)9 noted infarction in CT in as high as28.33% cases Table 3.

The incidence of ocular motor dysfunction hasbeen found to be in rising trend at par with CTfindings of hydrocephalus and rising levels ofCSF protein and cells and decreasing levels ofCSF sugar. This finding clearly points towardsthe role of severity of the inflammation in thepathogenesis of ocular complications and neurological deficits.

364 AIOC 2009 PROCEEDINGS

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365NEURO OPHTHALMOLOGY SESSION

References1. Verma BMD, Srivastav SK, Srivastav JR. Ocular

manifestation of tubercular meningitis and theirprognostic value in children. IJO. 1981;29:301-2.

2. Seth V.Neurotuberculosis II: Essentials oftuberculosis in children. Jaypee Brothers 1997.

3. Mishra RK, Gupta SP: JIMA 1962;38:513.

4. Kent SJ, Crowe SM, Yung A. Tubercular meningitis,a 30 year review. Clin Infect Dis. 1993;17;987-94.

5. Stewart SM.The bacteriological diagnosis of TBmeningitis. J Clin Patho, 1953;6:241-2.

6. Sumi MG et al. Rapid diagnosis of TB meningitis by

dot-immuno binding assay. Acta Neurol Scand. 2000,

61-64.

7. Banakappa DG. Study of TB meningitis. Ind Paed,

1993;20:421-33.

8. Ozates M et al., CT scan of brain in TB meningitis.

Acta Radiol. 2000;41:13-7.

9. Bhargav S et al., TB meningitis- a CT study. Br J

Radiol. 1982;55:189-96.

Discussion Comments by Virender Sachdeva: This study attempts to study a disease which is epidemic in India

but still a scant literature is available.The study appropriately describes the common presenting complaints. It also defines the incidence of commonfindings. In accordance with the present study, the available literature also states that the chief presenting complaintis decrease in vision followed by double vision. In a study by Verma et al, where they studied 50 cases of pediatricTubercular meningitis, they found 76 % had ophthalmic features. They also found that there is a frequent involvementof third nerve followed by sixth cranial nerve. However, as in the current study, there is no patient with a Superior oblique palsy ( SO palsy ). Their study also showed correlation with mortality apart from the other features mentionedin the current study. They found the highest incidence of mortality was with sixth nerve palsy ( probably as it maybe indicative of a increased intra-cranial pressure), followed by a complete third nerve palsy, presence of fixed,dilated pupils, semidilated pupils , presence of papilledema , and presence of choriodal tubercles( as they areindicative of military tuberculosis ).

In addition, as highlighted by the study doing a good neuro-imaging investigation can help further define the possiblenature of complications.

This therefore, calls for careful attention to recognizing these signs of ocular examination, however, limitation totreatment still exist.

Also, one must keep in mind that the patient with tubercular meninigitis may not have any ophthalmic manifestations

in beginning but may go on to develop an ATT ( ethambutol) induced toxicity during the course of treatment.

References: Verma B, Srivastava SK, Srivastava JR. Ocular manifestations of tubercular meningitis and their prognostic value in children, Indian J Ophthalmol 1981; 29: 301-2.

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