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TOPIC OF THE ISSUE- BRIEF REPORT
Year : 2010  |  Volume : 58  |  Issue : 5  |  Page : 732-735

Tuberculous optochiasmatic arachnoiditis


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

Date of Acceptance24-Jun-2010
Date of Web Publication28-Oct-2010

Correspondence Address:
M Alexander
Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu - 632 004
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.72194

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 » Abstract 

Arachnoiditis involving optic nerve and the optic chiasm can occur as a complication of tuberculous meningitis (TBM). This study evaluates the clinical features, cerebrospinal fluid (CSF) and laboratory parameters and imaging findings of optochiasmatic arachnoiditis (OCA) and also tried to identify any factors which can predict this complication in patients with TBM. Patients admitted with TBM in the neurology wards of a tertiary care teaching hospital over a period of 6 years formed the material for this study. Student's "t" test and univariate analysis were done to identify any predictors for this complication and the variables found to be significant were further analyzed by multivariate logistic regression analysis. One hundred sixty-three patients with TBM, admitted over a 6-year period, were studied. Twenty-three (14%) patients developed OCA. Eighteen out of 23 (78%) developed this complication while on antituberculous treatment (ATT) and 5/23 (22%) were newly diagnosed cases of TBM. Of those already on treatment, 12/23 (52%) were receiving only ATT, the remaining 6/23 (26%) had received steroids along with ATT in varying doses and duration. The average period from diagnosis of TBM to visual symptoms was 6.4 months. On the multivariate logistic regression analysis, female sex (P < 0.037), age less than 27 (P < 0.008) years and protein content in the CSF > 260 mg% (P < 0.021) were the factors predisposing toward this complication. At 6 months follow-up, on treatment with steroids and ATT, 17% had improvement and no further deterioration was noted in visual acuity in 52%. OCA can develop even while on treatment with ATT. Young women with a high CSF protein content seem to be more prone for this complication.


Keywords: Arachnoiditis, optic chiasm, tuberculous meningitis


How to cite this article:
Aaron S, Mathew V, Anupriya A, Sunithi M, Maya T, Goel M, Alexander M. Tuberculous optochiasmatic arachnoiditis. Neurol India 2010;58:732-5

How to cite this URL:
Aaron S, Mathew V, Anupriya A, Sunithi M, Maya T, Goel M, Alexander M. Tuberculous optochiasmatic arachnoiditis. Neurol India [serial online] 2010 [cited 2019 Oct 15];58:732-5. Available from: http://www.neurologyindia.com/text.asp?2010/58/5/732/72194



 » Introduction Top


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 Top


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 Top


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.
Figure 1: T1W gadolinium coronal and axial MRI images; multiple rounded and confluent ring and nodular enhancing lesions in the suprasellar cistern involving the opticochiasmatic region

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Figure 2: T1W Gadolinium coronal MRI images; multiple rounded and confluent ring and nodular enhancing lesions in the suprasellar cistern involving the opticochiasmatic region

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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].
Table 1: Severity of visual impairment in patients with symptomatic optochiasmatic arachnoiditis

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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].
Table 2: Clinical and radiological features

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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.
Table 3: Univariate analysis for continuous variables

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Table 4: Univariate analysis for fixed variables

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Table 5: Multivariate logistic regression analysis

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 » Discussion Top


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 Top

1.Weinstein GW, Powell SR, Thrush WP. Chiasmal neuropathy secondary to rheumatoid pachymeningitis. Am J Ophthalmol 1987;104:439-40.  Back to cited text no. 1
[PUBMED]    
2.Tang RA, Grotta JC, Lee KF, Lee YE. Chiasmal syndrome in sarcoidosis. Arch Ophthalmol 1983;101:1069-73.   Back to cited text no. 2
    
3.Purvin V, Herr GJ, De Myer W. Chiasmal neuritis as a complication of Epstein-Barr virus infection. Arch Neurol 1988;45:458-60.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Chakraborty AK. Epidemiology of tuberculosis: current status in India. Indian J Med Res 2004;120:248-76.   Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Thwaites GE, Chau TT, Stepniewska K, Phu NH, Chuong LV, Sinh DX, et al. Diagnosis of adult tuberculous meningitis by use of clinical and laboratory features. Lancet 2002;360:1287-92.   Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Bachani D, Limburg H. National Programme for Control of Blindness in India: Course material for training district programme management, New Delhi. Ophthalmic Section. Directorate General of Health Services, Ministry of Health and Family Welfare 1996. p. 169.  Back to cited text no. 6
    
7.Medical Research Council Report: Streptomycin treatment of tuberculous meningitis. Lancet 1948;1:582-96.  Back to cited text no. 7
    
8.Sinha MK, Garg RK, Anuradha HK, Agarwal A, Singh MK, Verma R, et al. Vision impairment in tuberculous meningitis: predictors and prognosis. J Neurol Sci 2010;290:27-32.  Back to cited text no. 8
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9.Schoeman JF, Van Zyl LE, Laubscher JA, Donald PR. Effect of corticosteroids on intracranial pressure, computed tomographic findings, and clinical outcome in young children with tuberculous meningitis. Pediatrics 1997;99:226-31.  Back to cited text no. 9
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10.Gourie-Devi M, Satish P. Hyaluronidase as an adjuvant in the treatment of cranial arachnoiditis (hydrocephalus and optochiasmatic arachnoiditis) complicating tuberculous meningitis. Acta Neurol Scand 1980;62:368-81.  Back to cited text no. 10
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11.Stefan DC, Andronikou S, Freeman N, Schoeman J. Recovery of vision after adjuvant thalidomide in a child with tuberculous meningitis and acute lymphoblastic leukemia. J Child Neurol 2009;24:166-9.   Back to cited text no. 11
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12.Navarro IM, Peralta VH, Leon JA, Varela EA, Cabrera JM. Tuberculous optochiasmatic arachnoiditis. Neurosurgery 1981;9:654-60.  Back to cited text no. 12
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13.Simmons CP, Thwaites GE, Quyen NT, Torok E, Hoang DM, Chau TT, et al. Pretreatment intracerebral and peripheral blood immune responses in Vietnamese adults with tuberculous meningitis: diagnostic value and relationship to disease severity and outcome. J Immunol 2006;176:2007-14.  Back to cited text no. 13
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14.Jakka S, Veena S, Rao AR, Eisenhut M. Cerebrospinal fluid adenosine deaminase levels and adverse neurological outcome in pediatric tuberculous meningitis. Infection 2005;33:264-6.  Back to cited text no. 14
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    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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