Acute Confusional Syndrome and Hypopituitarism Produced by a Giant Aneurysm of Internal Carotid Artery

Abstract

T he syndrome of pituitary insufficiency secondary to aneurysms of the internal carotid artery is uncommon, and the prevalence has been estimated in 0.17%. The first description was published by Mitchell in 1889, cited by Dussault et al. A 74-year-old woman presented with a 3-day history of progressive weakness and dizziness, nausea, and increasing confusion. Her medical history was only relevant for systemic hypertension. The examination revealed a conscious patient, disoriented, not obeying commands (Glasgow Coma Scale of 13/15), and having equal pupils, with no cranial nerves or motor limbs deficits. The remainder of the physical examination disclosed no abnormality in an afebrile, well-nourished, and wellhydrated patient. Serum and hematologic analyses showed a sodium level of 131 mmol/L and potassium of 3.7 mmol/L. Lumbar puncture and urinalysis were nonspecific. A brain computed tomography without contrast showed an eroded sella in its left half. Magnetic resonance imaging of the brain revealed an intraand left parasellar lesion, isointense on T1-weighted images and hypointense on T2-weighted images (Figure 1). Magnetic resonance angiography showed a 2.2 3 2.5 cm left cavernous internal carotid artery aneurysm. Cerebral angiography (Figure 2) showed a left carotid cavernous aneurysm with intrasellar extension. Basal endocrine studies showed hyperprolactinemia with decreased levels of thyrotropin, free T4, corticotropin, serum cortisol, insulin-like growth factor 1, follicle stimulating hormone, and luteinizing hormone. She started corticosteroids and levothyroxine. Conservative treatment was decided, and the patient was discharged home with replacement endocrine therapy for life. The pathogenesis of pituitary dysfunction induced by sellar and parasellar aneurysms remains uncertain. Two pathogenetic possibilities are postulated, and often, a combination of them is present. On one hand, compression and destruction of pituitary tissue by an expanding mass lesion might explain itself a decrease in the production of all pituitary hormones, including prolactin. On the other, compression of pituitary stalk or hypothalamic tissue compromising the delivery of hypothalamic factors would also explain hypopituitarism, inducing hyperprolactinemia as in our case and the majority of cases previously published.