Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 58, Num. 5, 2010, pp. 732-735

Neurology India, Vol. 58, No. 5, September-October, 2010, pp. 732-735

Topic of the Issue- Brief Report

Tuberculous optochiasmatic arachnoiditis

A Anupriya¹, M Sunithi², T Maya³, M Goel³, M Alexander³, S Aaron³, V Mathew³

¹ Neurology Unit, Department of Ophthalmology, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
² Neurology Unit, Department of Radiology, Christian Medical College & Hospital, Vellore, Tamil Nadu, India
³ Neurology Unit, Department of Neurological Sciences, Christian Medical College & Hospital, Vellore, Tamil Nadu, India

Correspondence Address:
M Alexander
Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu - 632 004
India
mathewalex@cmcvellore.ac.in

Date of Acceptance: 24-Jun-2010

Code Number: ni10199

PMID: 21045497

DOI: 10.4103/0028-3886.72194

Abstract

Keywords: Arachnoiditis, optic chiasm, tuberculous meningitis

Introduction

Optochiasmatic arachnoiditis (OCA) refers to inflammatory changes with exudates in the leptomeninges around the optic chiasm and the optic nerves. This can lead to a decrease in the visual acuity, with variable progression to partial or total blindness.

It is a condition with multiple etiologies, including rheumatoid pachymeningitis, ^[1] sarcoidosis, ^[2] Epstein-Barr viral infection, ^[3] etc.

In developing countries like India, with a high incidence of tuberculosis, ^[4] tuberculous meningitis (TBM) can be an important cause for development of this condition. There is a paucity of literature on this subject.

In this study we have focused on the clinical features of the subgroup of patients who developed OCA as a complication of TBM. We also tried to identify any factors which can predict this complication.

Materials and Methods

Patients admitted with TBM in the neurology wards of a tertiary care teaching hospital over a period of 6 years were included in the study. Their records and imaging studies were analyzed. Those who had an alternative diagnosis made after admission or other forms of chronic meningitis were excluded. The diagnosis of TBM was based on the criteria described by Thwaites et al. ^[5]

As part of the workup for chronic meningitis, cerebrospinal fluid (CSF) India Ink preparation and Cryptococcus antigen were done in all cases. CSF cytospin and flow cytometry was done in suspected cases of carcinomatous meningitis.

All the patients with OCA had magnetic resonance imaging (MRI) with gadolinium in addition to computerized tomography (CT) scan, and in those patients with clinical features of spinal involvement, an additional MRI imaging of the spine was done.

The visual impairment was categorized according to the standard World Health Organization (WHO) definition for visual impairment and also according to the criteria for National Program for Control of Blindness (NPCB) in India. ^[6] The Medical Research Council (MRC) staging ^[7] was used to categorize the severity of TBM [Stage I: fully conscious and no deficits; Stage II: minor neurological deficits (cranial nerve palsies) with no or slight impairment in sensorium; Stage IIII: severe clouding of sensorium with or without convulsions and severe paresis].

At admission, the best corrected visual acuity was noted using the Snellen's chart and pupillary light reflex was noted using the swinging flashlight test. Fundus examination was done by direct ophthalmoscope at admission and on subsequent OPD visits. In those patients continuing to be in MRC Stage III, absence of menace reflex and absence of aversion to bright light was classified as "Blind" according to WHO definition for visual impairment or "Social blindness" according to the NPCB criteria.

Statistical analysis was performed to compare patients who developed symptomatic OCA with those who did not develop this complication. Student's " t" test and univariate analysis were done and the variables found to be significant were further analyzed by multivariate logistic regression analysis.

Results

Totally 163 adult patients with TBM were studied. Of them, 84 (51.5%) were males and 79 (48.4%) were females. Mean age was 33.3 (±1.12) years. Twenty-three (14%) patients had OCA, [Figure - 1] and [Figure - 2] of whom 6 (26%) were males and 17 (74%) were females. The mean age of these patients was 24.52 (±1.96) years.

At the time of admission, 13/23 (56.5%) were in Stage II (MRC staging of TBM) and 10/23 (43.4%) were in Stage III. Also, 18/23 (78%) patients were already diagnosed cases of TBM receiving antituberculous treatment (ATT) and 5/23 (21%) were newly diagnosed cases.

Of the 18 patients who were already on ATT, 12 (52%) patients were being treated with ATT alone, and the remaining 6 (26%) had received steroids along with ATT for varying periods and doses. Also, 15/18 (83%) patients had good compliance to medications.

The mean interval between the diagnosis of TBM and the onset of visual symptoms was 6.4 (±1.27) months and the average duration of visual symptoms at the time of seeking treatment was 2.5 (±0.45) months.

The severity of visual impairment varied form mild (13%) to no perception of light (13%) [Table - 1].

Nineteen of 23 patients (82%) were blind according to the standard WHO definition for visual impairment. Also, 10/23 patients were in MRC Stage III. Of these, four improved to MRC stage II and the remaining six patients continued to have severely altered sensorium. All had absent menace and absent aversion to bright light and were classified as "Blind" according to WHO definition for visual impairment or "Social blindness" according to the NPCB criteria.

Patients with spinal involvement were divided into two categories [Table - 2].

Only spinal arachnoiditis

11/23(48%) had only lower motor neuron findings suggestive of asymmetrical radiculopathy. Seven of these patients had shown patchy gadolinium enhancement of the roots on MRI and the remaining four had normal imaging.

Associated myelopathy

3/23(13%) had features of upper motor neuron findings suggestive of spinal cord involvement with or without radiculopathy. These patients had patchy lesions in the cord with gadolinium enhancement MRI.

Of 163 patients, 4 had arachnoiditis seen on imaging in the optochiasmatic region without any visual symptoms.

None of the patients had an extrameningeal focus of tuberculosis or an immunocompromised state.

After diagnosing symptomatic OCA, 14/23 (61%) were treated with ATT (INH, Rifampacin, Ethambutol and Pyrazinamide) + oral steroids (dexamethasone 0.1 mg/kg/day in divided doses for 1 month and then a tapering schedule over the next 2 weeks). Nine of 23 patients (39%) were given ATT + IV Methylprednisolone 1 g for 3 days, followed by oral steroids.

Associated hydrocephalus (communicating type) was present in 11/23 patients. Nine of them underwent ventriculo-peritoneal shunt.

At 6 months follow-up, improvement in visual acuity (at least by one grade NPCB criteria) was seen in 4/23 (17%). Further worsening was noted in 5/23 (21%) patients and it was unchanged in 12/23 (52%) patients. Five out of 23 (21%) patients were lost for follow up. Of the nine patients who had undergone ventriculo-peritoneal shunt, improvement in vision was seen in two.

Clinical, radiological, CSF and other laboratory parameters were compared and analyzed in patients with TBM with and without OCA [Table - 3] and [Table - 4].

On the multivariate logistic regression analysis [Table - 5], female sex, younger age and a raised CSF protein content were identified as risk factors or predictors for developing this complication.

Discussion

In this study, we found OCA causing visual impairment in 14% of patients with TBM. A recent study from ^[8] India also shows OCA as the leading cause for visual impairment in patients with TBM. Once established, only 17% showed improvement with treatment, emphasizing the need to prevent this complication. Early recognition may be helpful because in 52% patients the vision did not deteriorate further with treatment.

Corticosteroids have been shown to improve both survival rate and neurological outcome in patients with TBM. Treatment with steroids for a month has shown to significantly decrease the basal exudates. ^[9]

It has to be noted that in this series, 78% of the patients had developed this complication while on ATT. Only 30% were receiving steroids.

Many treatment modalities have been tried in treating tuberculous arachnoiditis like intrathecal hyaluronidase, ^[10] thalidomide ^[11] and microsurgical intervention. ^[12]

This study also had identified younger age, female sex and a raised CSF protein as predictors for the development of this complication. The significantly high incidence of this complication in younger age group may be explained on the basis of a better immune response.

An exaggerated host response against tuberculous protein is thought to play an important role in this. Simmons et al. ^[13] found that in patients with TBM, CSF concentrations of IL-6 were independently associated with significant neurological deficit. In a prospective study from South India, ^[14] children having TBM with neurological deficit had significantly higher CSF adenosine deaminase (ADA) levels compared with controls. The significantly elevated protein content in the CSF could indicate a more intense tissue reaction mediated by immunity.

In conclusion, while treating patients with TBM, one needs to anticipate this complication especially in young female patients with high CSF protein. Starting corticosteroids along with ATT may help in preventing this complication.

References

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