Cognitive Function and Cerebral Assessment in Patients Who Have Cushing’s Syndrome Isabelle Bourdeau, MD a, * , Ce´line Bard, MD b , He´le`ne Forget, PhD c , Yvan Boulanger, PhD d , Henri Cohen, PhD e , Andre´ Lacroix, MD a a Division of Endocrinology, Department of Medicine, Ho ˆtel-Dieu du Centre Hospitalier de l’Universite´ de Montre ´al, 3840 Saint-Urbain Street, Montreal, QC H2W 1T8, Canada b Department of Radiology, Ho ˆtel-Dieu du Centre Hospitalier de l’Universite´ de Montre ´al, 3840 Saint-Urbain Street, Montreal, QC H2W 1T8, Canada c Department of Psychology, Universite´ du Que´bec en Outaouais, 283 Alexandre Tache ´, CP 1250, suc. Hull, Gatineau, QC J8X 3X7, Canada d Department of Radiology, Ho ˆpital Saint-Luc du Central Hospitalier de l’Universite ´ de Montre ´al, 1058 St-Denis, Montreal, QC H2X 3J4, Canada e Cognitive Neuroscience Center, Universite ´ du Que ´bec a ` Montre ´al, P.O. Box 8888, Succ. Centre-Ville, Montreal, QC H3C 3P8, Canada Corticosteroids play an important role in the function and homeostasis of the central nervous system (CNS). Chronic exposure to supraphysiologic levels of glucocorticoids (GCs) in Cushing’s syndrome (CS) is associated with an increased prevalence of sleep disturbances, mood alterations, psychiatric diseases, cognitive impairment, and anatomical brain changes. Thus, patients who have CS provide a natural model to demonstrate the interactions between hypercortisolism and brain function in people. This article presents data on alterations of brain anatomy and metabolism and cognitive and neuropsychologic impairments for patients who have CS. Loss of brain volume in endogenous Cushing’s syndrome Previous pathologic and imaging studies suggested that some morphologic anatomic modifications did occur in the brain of patients who have CS. The authors first wish to point out that the terminology cerebral atrophy has been * Corresponding author. E-mail address: isabelle.bourdeau@umontreal.ca (I. Bourdeau). 0889-8529/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ecl.2005.01.016 endo.theclinics.com Endocrinol Metab Clin N Am 34 (2005) 357–369