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Year : 2010  |  Volume : 58  |  Issue : 5  |  Page : 714-715

Optochiasmatic arachnoiditis and neurotuberculosis: Prognostic indicators and therapeutic strategies

Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India

Date of Acceptance07-Sep-2010
Date of Web Publication28-Oct-2010

Correspondence Address:
M Gourie-Devi
Department of Neurology, Institute of Human Behaviour and Allied Sciences, Dilshad Garden, New Delhi - 110 095
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.72174

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 » Abstract 

Tuberculous meningitis (TBM) is a serious meningitic infection commonly found to occur in the developing countries endemic to tuberculosis. Based on the clinical features alone, the diagnosis of TBM can neither be made nor excluded with certainty. Unfortunately there is still no single diagnostic method that is both sufficiently rapid and sensitive. Most factors found to correlate with poor outcome can be directly traced to the stage of the disease at the time of diagnosis. The only way to reduce the mortality and morbidity is by early diagnosis and timely recognition of complications and institution of the appropriate treatment strategies.

Keywords: Optochiasmatic arachnoiditis, antituberculous drugs, elevated intracranial pressure, hydrocephalus, tuberculoma, tuberculous meningitis, vasculitis

How to cite this article:
Gourie-Devi M. Optochiasmatic arachnoiditis and neurotuberculosis: Prognostic indicators and therapeutic strategies. Neurol India 2010;58:714-5

How to cite this URL:
Gourie-Devi M. Optochiasmatic arachnoiditis and neurotuberculosis: Prognostic indicators and therapeutic strategies. Neurol India [serial online] 2010 [cited 2022 Oct 2];58:714-5. Available from: https://www.neurologyindia.com/text.asp?2010/58/5/714/72174

Impairment of vision in tuberculous meningitis (TBM) can be due to a variety of causes, including primary involvement of optic nerve by tuberculous lesion leading to optic neuritis, optochiasmatic arachnoiditis (OCA), tuberculoma in the chiasmatic region or in the optic pathways, chorioretinitis, secondary to hydrocephalus and increased intracranial pressure, and finally due to ethambutol toxicity. In the past, sequelae of visual impairment had been reported in 35% of TBM patients. [1] It may be recalled that this was in the era when rifampicin had not yet come into vogue, but surprisingly the frequency of visual impairment has not significantly decreased over the last 5 decades. In a recent study from India, Sinha et al.[2] reported that 27% of TBM patients had decreased vision and the main causes were OCA and optochiasmal tuberculoma, and in this issue of Neurology India, Aaron et al.[3] report a figure of 14% with OCA. It is also important to recognize that OCA can be caused by neurocysticercosis, sarcoidosis, and subarachnoid hemorrhage. In patients presenting with isolated OCA without overt evidence of tuberculosis, if investigations for tuberculous etiology do not yield positive results, appropriate investigations have to be done to look for other causes. However, it must be emphasized that in India and in other developing countries tuberculosis is the most common cause of OCA.

Dastur et al.[4] in a seminal publication elaborating the pathologic features in TBM observed that the basal exudate was most prominent in the interpeduncular fossa, over the floor of the third ventricle and around the optic chiasma. The exudate in the majority of cases was dense and sometimes even firm and plaque-like, whereas only in a few it formed a thin layer. The exudates may compress and occlude vascular supply of optic nerve and chiasma and also cause vasculitis.

The impairment of vision in OCA is of insidious onset and slowly progressive but rarely it can be of sudden onset and may be unilateral or bilateral and in severe cases there may be blindness. The visual loss is attributed to compression or ischemia or to both mechanisms and sudden visual loss may be due to compromise of blood supply or rarely to paradoxical reaction during antitubercular treatment (ATT) following withdrawal of steroids. [5] Reliable method of establishing the diagnosis of OCA on magnetic resonance imaging (MRI) with contrast are features of perichiasmal enhancement and hypertrophy of chiasma and cisternal segment of optic nerves. [6],[7] Aaron et al.[3] reported confluent enhancing lesions in suprasellar cistern in the chiasmatic region. The associated hydrocephalus has often been observed in many patients.

Treatment of OCA continues to be a challenge and the response is generally not satisfactory. ATT in combination with steroids does result in restoring proper vision in some patients. However, it is noteworthy that OCA can also occur while on ATT and steroids. [3] Various surgical procedures, such as shunt surgery for hydrocephalus and microsurgical decompression of optic chiasm and optic nerves, yielded encouraging results in a few patients. [8],[9] Gourie-Devi and Satish reported the use of intrathecal hyaluronidase as an adjuvant in the treatment of hydrocephalus and OCA and on comparison with shunt surgery observed improvement of vision in three of the seven patients treated with intrathecal hyaluronidase as against one of the six patients with shunt surgery. [10] Schoeman et al.[11] described that adjuvant thalidomide therapy had led to dramatic recovery of vision in four patients with blindness due to OCA.

The prognosis in most of the cases with impairment of vision in TBM remains poor; therefore, it is important to identify predictors of occurrence. Sinha et al. identified papilledema, cranial nerve paralysis, raised cerebrospinal fluid (CSF) protein, and OCA on MRI to be the predictors of deterioration of vision, and Aaron et al. report that young women and cases with high CSF protein appear to be more susceptible to develop OCA. [2],[3]

Visual impairment and OCA are common complications of TBM and since ATT, steroids, surgery, or adjuvants are not effective in many instances, there is a need to examine the underlying mechanisms, develop strategies to prevent this dreaded complication, and explore novel methods of treatment.

 » References Top

1.Miettinen P, Wasz-Hocket O. Late ophthalmological sequelae of tuberculous meningitis. Acta Pediatr 1962;51:43-52.  Back to cited text no. 1
2.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. 2
3.Aaron S, Alexander M, Mathew V, Anupriya A, Sunithi M, Maya T,et al. Tuberculous optochiasmatic arachnoiditis. Neurol India 2010;58:732-5.  Back to cited text no. 3
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4.Dastur DK, Lalitha VS, Udani PM, Parekh U. The brain and meninges in tuberculous meningitis - Gross pathology in 100 cases and pathogenesis. Neurol India 1970;18:86-100.  Back to cited text no. 4
5.Monga PK, Dhaliwal U. Paradoxical reaction in tuberculous meningitis resulting in involvement of optic radiation. Indian J Ophthalmol 2009;57:139-41.  Back to cited text no. 5
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6.Silverman IE, Liu GT, Bilaniuk LT, Volpe NJ, Galetta SL. Tuberculous meningitis with blindness and perichiasmal involvement on MRI. Pediatr Neurol 1995;12:65-7.  Back to cited text no. 6
7.Chang KH, Han MH, Roh JK, Kim IO, Han MC, Choi KS,et al. Gd-DTPA enhanced MR imaging in intracranial tuberculosis. Neuroradiology 1990;32:19-25.  Back to cited text no. 7
8.Bhagwati SN. Ventriculo-atrial shunt in tuberculous meningitis with hydrocephalus. J Neurosurg 1971;35:309-13.  Back to cited text no. 8
9.Scott RM, Sonntag VK, Wilcox LM, Adelman LS, Rockel TH. Visual loss from optochiasmatic arachnoiditis after tuberculous meningitis. Case report. J Neurosurg 1977;46:524-6.  Back to cited text no. 9
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
11.Schoeman JF, Andronikou S, Stefan DC, Freeman N, van Toom R. Tuberculous meningitis-related optic neuritis: Recovery of vision with thalidomide in 4 consecutive cases. J Child Neurol 2010;25:822-8.  Back to cited text no. 11

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