title: Pituitary stalk lesions: the Mayo Clinic experience.
abstract: BACKGROUND
  Pituitary stalk lesions have various etiologies, often not clinically apparent. Pathological samples from these lesions are rarely obtained, because of the critical location and function of the hypophyseal stalk.
  
  
  OBJECTIVE
  The purpose of this study was to characterize the etiological spectrum of pituitary stalk lesions seen at Mayo Clinic Rochester over 20 years and to determine whether specific magnetic resonance imaging (MRI) characteristics could provide clinician guidance with regard to the etiology of infundibular lesions.
  
  
  METHODS
  A retrospective review of patients with pituitary stalk lesions seen at Mayo Clinic Rochester between 1987 and 2006 was conducted. Demographic, clinical presentation, imaging, laboratory, operative, and pathology data were reviewed and are reported using descriptive statistics.
  
  
  RESULTS
  Of the 152 pituitary stalk lesions included, 49 (32%) were neoplastic, 30 (20%) were inflammatory, 13 (9%) were congenital anomalies, and 60 (39%) were of unclear etiology. Diabetes insipidus was diagnosed in 43 (28%) of the 152 patients, and 49 (32%) patients had at least one anterior pituitary hormone deficit. Secondary hypogonadism was the most common endocrine deficiency. Eleven of 13 congenital lesions were round in appearance and 5 of 7 patients with neurosarcoidosis confirmed by pathology had a uniformly thickened pituitary stalk on MRI. There were no statistically significant correlations between hypopituitarism and the pattern of enhancement or size of the lesion.
  
  
  CONCLUSIONS
  Findings on MRI remain key in guiding the diagnosis of pituitary stalk lesions, particularly when used in conjunction with other clinical clues. There are no good imaging predictors for hypopituitarism, making clinical evaluation of all patients with pituitary stalk lesions crucial.
authors.affiliation: Division of Endocrinology, Mayo Clinic Rochester, 200 First Street Southwest, Rochester, Minnesota 55905, USA.
authors.forename: Adina F
authors.initials: AF
authors.lastname: Turcu
authors.forename: Bradley J
authors.initials: BJ
authors.lastname: Erickson
authors.forename: Eleanor
authors.initials: E
authors.lastname: Lin
authors.forename: Sonsoles
authors.initials: S
authors.lastname: Guadalix
authors.forename: Kara
authors.initials: K
authors.lastname: Schwartz
authors.forename: Bernd W
authors.initials: BW
authors.lastname: Scheithauer
authors.forename: John L D
authors.initials: JL
authors.lastname: Atkinson
authors.forename: William F
authors.initials: WF
authors.lastname: Young
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002648:Child; D002675:Child, Preschool; D003919:Diabetes Insipidus / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007006:Hypogonadism / Q000209:etiology; D033162:Incidental Findings; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010900:Pituitary Diseases / Q000097:blood / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D010902:Pituitary Gland / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D010908:Pituitary Hormones, Anterior / Q000097:blood / Q000172:deficiency / Q000378:metabolism; D010911:Pituitary Neoplasms / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D012189:Retrospective Studies; D055815:Young Adult
chemical_list: D010908:Pituitary Hormones, Anterior