Microprolactinoma with visual field defect: An unsuspected etiology
A 32-year-old female patient presented to our department with history of headache, oligomenorrhea, and galactorrhoea for 2 years duration. The headache was located in the frontotemporal region with maximal intensity during the morning hours. She denied a history of vomiting, diplopia, or blurring of vision. She gave birth to 2 children with last childbirth about 7 years back. There was no history to suggest thyroid dysfunction, systemic or psychiatric ailment, and drug intake. Examination revealed normal vital parameters with a body mass index of 21.2 kg/m2 and there was no evidence of goiter. Her visual field examination by confrontation tests was apparently normal and she had no neurological deficit. Fundus examination showed mild pallor and was considered normal. Hormonal profile revealed hyperprolactinemia (serum prolactin – 1228 ng/mL) with normal thyroid and gonadal axes evaluation. Dynamic and contrast enhanced MRI study of the sella and pituitary gland showed well-defined intra-sellar mass of 0.8 × 0.4 × 0.6 cm3 over the left side of the pituitary gland without any supra-sellar extension and not in contact with the optic chiasm. There is mild thickening of the pituitary stalk with homogenous hyper-intensity in post-contrast images [Figure –].\nShe was diagnosed as a case of microprolactinoma and managed with 0.5 mg of cabergoline twice weekly. She showed clinical improvement in the form of regular menses and cessation of galactorrhoea. Her headache did not improve as we had expected and we continued her with cabergoline for another 6 months. Her repeat prolactin was normal and she continued to complain of headache and occasional blurring of vision. In view of persisting symptoms, a repeat neuro-imaging was done which revealed pituitary microadenoma (0.6 × 0.5 cm2) as described previously. Visual field examination revealed marked constriction of peripheral vision [] and bilateral early papilledema. Evaluation of the cortical venous sinuses by magnetic resonance venography revealed all patent sinuses. She was considered to have intra-cranial hypertension of obscure etiology and a guarded lumbar puncture was done after giving mannitol and acetazolamide. Her opening CSF pressure was 25-mm Hg and biochemical evaluation of the CSF was normal. She was diagnosed as a case of IIH and treated with acetazolamide along with cabergoline. Her symptoms and headache improved markedly and repeat perimetry showed completely normal visual fields [Figure and ]. During the last follow-up, she is asymptomatic with no headache, visual defect, diplopia, and normal fundus examination.