A 22 yr old lady, presented to us with history of sudden onset loss of vision in both the eyes with painful eye movements of one month duration. She could not read recognise objects, and could perceive just rays of light. There was no history of headache, vomiting, altered sensorium. She did not have hearing loss, facial deviation, nasal regurgitation, weakness of limbs or involuntary movements. No history of fever,cough,loss of weight. No history of loose stools,vomiting,dysuria. No past history of hypertension,diabetes mellitus,tuberculosis,cerebrovascular accidents. There were no similar complaints or morbid illness in her family. She was married and had two children. There was no history of abortion. Her menstual history was normal. She did not have any high risk sexual behavior. Her diet was poor in carbohydrates and proteins. She did not have any addictions and did not consume any toxic substance. From the history, we made a provisional diagnosis of optic neuropathy. Infectious etiologies like tuberculosis,retroviral infection, CMV, toxoplasmosis were the primary differential diagnoses. A possibility of intracranial space occupying lesion was also considered.
On examination, she was poorly nourished with a BMI of 16 kg/m2. She was pale. Axillary lymphnodes were enlarged bilaterally, 3-4 in number on each side, largest of them measuring 4 x 5 cm-firm, palpable and matted. Examination of eyes showed normal eyelids, conjuctiva, cornea with relative afferent pupillary defect and normal light reflex (Fig. 1). Optic fundii examination showed chalky white disc with well demarcated margins and vessels suggestive of bilateral primary optic atrophy (Fig. 2Figs. 2 and 3 ). Extra ocular movements were normal. Other cranial nerves and sensorimotor system was within normal limits. There were no signs of meningeal irritation. Respiratory, Cardiovascular, Gastrointestinal systems examination revealed no abnormalities.
Haematological investigations revealed anaemia with elevated ESR, as depicted in Table 1 below.
Renal, liver function tests, serum electrolytes, blood sugar and urine routine examination were within normal limits. Chest x-ray was normal. Mantoux test was done to look for a tuberculous etiology which turned out to be strongly positive (20 x 20 mm). Suspecting tuberculous meningitis lumbar puncture done and cerebrospinal fluid analysis(CSF) showed normal opening pressure -160 mm H20, a normal appearance, elevated protein-256 mg/dl, low sugar 36 mg/dl. CSF contained 200 cells with 100 percent lymphocytes consistent with tuberculous meningitis. CSF Adenosine deaminase was 20 U/L(Positive)(Normal value <10U/L). Polymerase chain reaction for Mycobacterium tuberculosis was positive in CSF. Gram stain,India ink stain,Cryptococcal antigen test,fungal culture were negative in CSF. Fine needle aspiration cytology from axillary lymphnode showed only reactive hyperplasia. Axillary lymphnode biopsy showed caseating granulomatous and lymphadenitis consistent with tuberculosis.Toxoplasma, cytomegalovirus, VDRL and herpes serology were negative.Blood and urine cultures did not show any growth.Rheumatoid factor and antinuclear antibody was negative. Sickling test was negative.Neuroimaging showed pachy and leptomeningitis with no evidence of papilledema, but a thinned out optic nerve (Fig. 4 ).
So we made a final diagnosis of tuberculous meningitis with primary optic atrophy possibly as a complication of retro bulbar optic neuritis.
She was started on antituberculous drug regimen with isoniazid, rifampin, pyrazinamide & ofloxacin (substituted for ethambutol) along with steroids.Though her visual loss persisted, her general condition improved and she is on regular follow up.