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

AUTHORSS 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: anitmisra@gmail.com

Dr. Anita Misra, Prof. Madhumati Misra, Prof. Himansu Kumar Rajguru, Dr. Prasant Kumar Nanda
(Presenting Author: Dr. Anita Misra)

BM (Tubecular Meningitis) is the most dangerous form of tuberculosis infection and still the commonest chronic CNS infection in developed countries. In adults, it may occur as primary disease, accounts for 9.1% of extra pulmonary TB cases (Nelson 2004) or secondary to pulmonary TB. Diverse ocular manifestations occur as sequlae of TBM, due to chronically raised ICT or retinal vasculitis, in about 70% cases, up to 25% cases show oculocranial polyneuropathy.1 Ocular manifestation may be the presenting feature, analyses of which help

Tuberculous infection usually reaches the meninges by hematogenous route or through intracranial lymphatic from the cervical nodes. Bacilli are immobilized in end arteries and lead to submeningeal tubercular foci which discharge bacilli into subarachnoid space intermittently, causing perivascular exudation followed by caseation, gliosis, giant cell proliferation and vaculitis. The major impact falls on basal meninges (thick exudation surrounds cranial

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

NEURO OPHTHALMOLOGY SESSION Table-1: Systematic features of TBM patients at presentation (n=60 patients)
Prodromal symptoms Fever Cough Anorexia Vomiting Seizure Patients(n) 38 26 28 32 18 3 22 8 Signs of meningitis Altered sensorium Neck rigidity Kernigs sign Hypotension

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Sl. No. 1 2 3 4 5 6 7 8

Patients(n) 10 42 6 1 0 42

Weight loss Headache Motor paresis

Motor deficit

Involuntary movement Ocular palsies Defective vision

23

Cranial nerves II

Table-2: TBM cases with oculocranial nerve involved at presentation (n=60 patients)
Commonest presentations visual function Patients(n) 13 9 4 II nerve Vision Commonest presentations <6/18 6/18 Absent PL

40

Patients (n) 32 16 8 12 12 9 7 2 6

IV Combined VII VI

III

Ptosis Lagophthalmos Multiple Squint

11 12

Field Fundus

Scotoma Normal

Blind spot enlargement color vision Papilloedema

14

Papillitis

Primary OA

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

Normal Hilar nodes Patient (n) 25 19 X-ray chest Miliary shadow 9 Consolidation 0 Normal 18 Hydrocephalus 32 Basal enhancement 0

Secondary OA

18

Enhanced CT

Infarct 4

Tuberculoma 6

CSF analysis for TBM was positive in 48 (80%) cases as out lined in Table 4. Examination Appearance Clear <50 Patients(n) 12 12 20 28 26 12 10 Examination

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

Protein level/mg(%) <100 101-500 <40

Patients(n) 12 8 4 22 32 38 8

Xanthochromic Cobweb 51-100 >200

Cell count/mm3

501-1000 Sugar level/mg(%) AFB stain >1000 >40 -ive +ive

101-200

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

Classically TBM evolves through 3 stages as defined by British Council2 as (a) prodromal stage for 2-3 wks, (b) stage of meningeal irritation and (c) stage of cerebral involvement(symptoms of raised intracranial pressure, focal neurological

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deficits , cranial nerve palsies; usually II, III, IV, VI, VII, posterior fossa meningitis, spinal leptomeningitis, lastly coma, decorticating posture or extensor rigidity with dilated fixed pupils .Papillitis is the commonest neuroophthalmic complication in 60% cases but uveitis and choroid tubercles are rare due to their different pathogenesis).3 Diagnosis of TBM depends on high index of clinical suspicion, contact history, immunosuppression,chest X-ray,CT scan/MRI of brain and orbit may show nodular enhancing lesion with central hypodensity, central edema, infarctions, hydrocephalus and multiple intracranial tuberculomas. CSF analysis and culture is the key to diagnosis of TBM. Faintly visible spiders web clot due to CSF hyper proteinemia, low sugar with pleocytosis are almost pathognomonic. Acid fast bacilli are seen in CSF in less than 5% cases and culture positive in less than 10%.2,4,5

In the present study, out of 60 cases, 60% were male and 40% female.20%were below 20 yrs, 9% were above 60y, maximum cases of 28(46%) in 20-40 age group. Highest ocular sequel was seen in 40-60 age group and least complication were seen in 0-20 years of age. 39(65%) had definite contact history. Low grade fever was the commonest presenting symptom in 38(63%). Kerning sign of meningeal irritation was the commonest presenting sign in 42(70%) [Table-1] similar to 81% by Benakappa et.al. 1983.7 Common neuro ophthalmic complications noted were defective vision in 40(66.6%), diplopia in 13(21.6%). Table-2 shows the pattern and incidence of cranial nerve involvement (isolated and combined) in TBM, which is widely variable in different reported series. The commonest single cranial nerve involved was VI nerve in 11(18%) cases; combined palsy was the commonest pattern in 12(20%) cases. The commonest pattern of optic nerve involvement was optic atrophy (POA, SOA) in 25(42%) cases possibly due to late detection of cases, earlier presentations were papilloedema in 20%, papillitis in 15%, visual field defects in 18%. Radiological study of chest showed findings suggestive of pulmonary TB in 35 (54%), mostly hilar lymphadenopathy in 19(31.6%), but was normal in 25(46%) cases suggesting extra pulmonary TBM outlined in Table 3.

ophthalmologist can assist the neurophysician on reaching a definite diagnosis and in reducing morbidity and mortality due to TBM by early institution of appropriate therapy.

Retrospective analysis of the presenting Neuroophthalmic features of diagnosed cases of TBM and correlating with imaging and CSF findings. 60 proven cases of TBM having neuroophthalmic symptoms referred to our neuro-ophthalmology section from the depts. like Medicine. Paed. TB/Chest, Neurology, Neurosurgery between July 2005 and Feb 2008 were analyzed to describe the demography, Clinical profile, CSF analysis, radiological and imaging study along with detailed neuroophthalmic findings. Attempt has been made to correlate these manifestations of TBM with each other.

Dot immunobinding assay (Dot-Iba) for circulating antimicrobial antibodies in CSF is used for rapid diagnosis.6

Materials and Methods

All patients had received standard ATT and steroids. Symptomatic treatment given in all patients included mannitol, antibiotics, IV fluids, antipyretics and physiotherapy. Despite recent advances in Chemotherapy, TBM caused by typical/atypical mycobacterium remains a serious medical problem. Clinical and investigation procedures may be nonspecific and bacteriological proof difficult to obtain. An

Enhanced CT Scan revealed normal result in 18(30%), hydrocephalus was commonest finding in 32 (53.3%). Hydrocephalus was reported by Ozates et al. (2000)8 in 80% cases. CT evidence of tuberculomas was noted in 10% cases and infarction in 6.6% cases, however, Bhargava et. al. (1982)9 noted infarction in CT in as high as 28.33% cases Table 3.

Discussion

The incidence of ocular motor dysfunction has been found to be in rising trend at par with CT findings of hydrocephalus and rising levels of CSF protein and cells and decreasing levels of CSF sugar. This finding clearly points towards the role of severity of the inflammation in the pathogenesis of ocular complications and neuro logical deficits.

NEURO OPHTHALMOLOGY SESSION

1. Verma BMD, Srivastav SK, Srivastav JR. Ocular manifestation of tubercular meningitis and their prognostic value in children. IJO. 1981;29:301-2. 2. Seth V.Neurotuberculosis II: Essentials of tuberculosis 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 TB meningitis. J Clin Patho, 1953;6:241-2.

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References

6. Sumi MG et al. Rapid diagnosis of TB meningitis by dot-immuno binding assay. Acta Neurol Scand. 2000, 61-64. 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. 7. Banakappa DG. Study of TB meningitis. Ind Paed, 1993;20:421-33.

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 common findings. In accordance with the present study, the available literature also states that the chief presenting complaint is decrease in vision followed by double vision. In a study by Verma et al, where they studied 50 cases of pediatric Tubercular meningitis, they found 76 % had ophthalmic features. They also found that there is a frequent involvement of 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 mentioned in the current study. They found the highest incidence of mortality was with sixth nerve palsy ( probably as it may be 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 are indicative of military tuberculosis ). In addition, as highlighted by the study doing a good neuro-imaging investigation can help further define the possible nature of complications. This therefore, calls for careful attention to recognizing these signs of ocular examination, however, limitation to treatment 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.