Memory impairment in Cushing's disease.

Department of Neurology, IRCCS C. Mondino, University of Pavia, Italy.
Acta Neurologica Scandinavica (Impact Factor: 2.44). 02/1993; 87(1):52-5. DOI: 10.1111/j.1600-0404.1993.tb04075.x
Source: PubMed

ABSTRACT In the present study the cognitive performance of 25 patients with Cushing's disease (CD) was extensively evaluated in comparison with normal control subjects, matched one by one. The results indicate a selective impairment of memory functions: the number of patients showing a significantly impaired mnesic performance increases with age. Moreover, the neuropsychological impairment tends to recover in those cases who underwent further controls after surgical treatment. The neuropsychological data are discussed in the light of recent evidence in the literature concerning the effects of adrenal steroids on the brain.


Available from: Roberto Attanasio, Apr 17, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Endogenous Cushing's syndrome is an endocrine disease resulting from chronic exposure to excessive glucocorticoids produced in the adrenal cortex. Although the ultimate outcome remains uncertain, functional and morphological brain changes are not uncommon in patients with this syndrome, and generally persist even after resolution of hypercortisolemia. We present an adolescent patient with Cushing's syndrome who exhibited cognitive impairment with brain atrophy. A 19-year-old Japanese male visited a local hospital following 5 days of behavioral abnormalities, such as money wasting or nighttime wandering. He had hypertension and a 1-year history of a rounded face. Magnetic resonance imaging (MRI) revealed apparently diffuse brain atrophy. Because of high random plasma cortisol levels (28.7 μg/dL) at 10 AM, he was referred to our hospital in August 2011. Endocrinological testing showed adrenocorticotropic hormone-independent hypercortisolemia, and abdominal computed tomography demonstrated a 2.7 cm tumor in the left adrenal gland. The patient underwent left adrenalectomy in September 2011, and the diagnosis of cortisol-secreting adenoma was confirmed histologically. His hypertension and Cushingoid features regressed. Behavioral abnormalities were no longer observed, and he was classified as cured of his cognitive disturbance caused by Cushing's syndrome in February 2012. MRI performed 8 months after surgery revealed reversal of brain atrophy, and his subsequent course has been uneventful. In summary, the young age at onset and the short duration of Cushing's syndrome probably contributed to the rapid recovery of both cognitive dysfunction and brain atrophy in our patient. Cushing's syndrome should be considered as a possible etiological factor in patients with cognitive impairment and brain atrophy that is atypical for their age.
    Neuropsychiatric Disease and Treatment 09/2014; 10:1763-7. DOI:10.2147/NDT.S70611 · 2.15 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Biological studies of posttraumatic stress disorder (PTSD) have found alterations of physiological stress pathways [sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis] soon after trauma in individuals who have subsequently developed PTSD, leading researchers to hypothesize that pharmacological manipulation of stress hormone levels may aid in preventing the development of post-traumatic distress. The present paper first reviews the current understanding of the neurobiology of PTSD development and then provides the rationale and evidence for early pharmacological strategies to prevent/reduce post-traumatic distress in at-risk trauma victims. Emphasis is placed on those interventions targeting the SNS and the HPA axis. Furthermore, in light of recent calls to move away from categorical diagnostic outcomes, we discuss how examining post-traumatic distress from a transdiagnostic viewpoint may inform novel chemoprophylactic approaches (intervening pharmacologically after trauma to prevent post-traumatic distress). Current evidence is suggestive for medications, such as propranolol, hydrocortisone, morphine, and oxytocin, impacting early stress hormone levels and subsequent risk for post-traumatic distress; however, future research is needed prior to adapting recommendations for widespread use of any chemoprophylactic treatments.
    CNS Drugs 02/2014; DOI:10.1007/s40263-014-0145-7 · 4.38 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Disorders of the adrenal glands frequently have secondary neurological manifestations, while some diseases that involve the central nervous system are accompanied by adrenal gland dysfunction. Excessive corticosteroid secretions in primary or secondary Cushing's syndrome causes muscle weakness and behavioral disturbances, such as emotional lability and sometimes depression, while adrenal insufficiency may cause fatigue, weakness, and depression. Adrenoleukodystrophy and adrenoneuromyelopathy are X-linked recessive disorders of the metabolism of very long chain fatty acids that manifest with white matter abnormalities of the brain, myelopathy and/or neuropathy, as well as adrenal insufficiency. Other disorders of the adrenal glands include hyperaldosteroidism, which may cause weakness from hypokalemia. Dysfunction of the adrenal medulla causes excessive or deficient secretion of catecholamines, primarily causing cardiovascular symptoms. This chapter reviews the clinical manifestations and diagnostic aspects and treatment of the various disorders of the adrenal glands. Some of the congenital adrenal diseases are also discussed.
    Handbook of Clinical Neurology 01/2014; 120:749-71. DOI:10.1016/B978-0-7020-4087-0.00050-4