The brain as a target for adrenocortical steroids: Cognitive implications

Martignoni, E.; Costa, Alfredo; Sinforiani, Elena; Liuzzi, Antonio; Chiodini, P. G.; Mauri, M.; Bono, Giorgio; Nappi, Giuseppe

doi:10.1016/0306-4530(92)90040-e

Cited by 123 publications

(61 citation statements)

References 47 publications

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“…One study did neither describe diagnostic nor remission criteria (20). Described diagnostic criteria were clinical features (truncal obesity, skin and muscle arthophy, moon facies) (11,12,13,21), elevated urinary free cortisol (UFC) (11,12,13,21,22,23,24,25,26,27,28,29), elevated cortisol secretion rates (11,12,13,21,23,24,25,30), elevated midnight salivary cortisol (29,31), absence of blunted circadian rhythm of cortisol secretion (11,12,13,21,26,27,30,32,33), elevated ACTH levels (in CD only) (12,13,21,23,24), lack of suppression after low dose dexamethasone ((1 mg) (22,25,29,33), (2 mg) (12,13,21...…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Cushing's syndrome causes irreversible effects on the human brain: a systematic review of structural and functional magnetic resonance imaging studies

Andela

Haalen

Ragnarsson

et al. 2015

European Journal of Endocrinology

150

129

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Background: Cushing's syndrome (CS) is characterized by excessive exposure to cortisol, and is associated with both metabolic and behavioral abnormalities. Symptoms improve substantially after biochemical cure, but may persist during long-term remission. The causes for persistent morbidity are probably multi-factorial, including a profound effect of cortisol excess on the brain, a major target area for glucocorticoids. Objective: To review publications evaluating brain characteristics in patients with CS using magnetic resonance imaging (MRI). Methods: Systematic review of literature published in PubMed, Embase, Web of Knowledge, and Cochrane databases. Results: Nineteen studies using MRI in patients with CS were selected, including studies in patients with active disease, patients in long-term remission, and longitudinal studies, covering a total of 339 unique patients. Patients with active disease showed smaller hippocampal volumes, enlarged ventricles, and cerebral atrophy as well as alterations in neurochemical concentrations and functional activity. After abrogation of cortisol excess, the reversibility of structural and neurochemical alterations was incomplete after long-term remission. MRI findings were related to clinical characteristics (i.e., cortisol levels, duration of exposure to hypercortisolism, current age, age at diagnosis, and triglyceride levels) and behavioral outcome (i.e., cognitive and emotional functioning, mood, and quality of life). Conclusion:Patients with active CS demonstrate brain abnormalities, which only partly recover after biochemical cure, because these still occur even after long-term remission. CS might be considered as a human model of nature that provides a keyhole perspective of the neurotoxic effects of exogenous glucocorticoids on the brain.

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Section: European Journal Of Endocrinologymentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Cushing's syndrome causes irreversible effects on the human brain: a systematic review of structural and functional magnetic resonance imaging studies

Andela

Haalen

Ragnarsson

et al. 2015

European Journal of Endocrinology

150

129

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“…Partial improvement of several memory functions have been observed in small groups [121,125], correlated in one study with recovery of hippocampus volume [126], but not in the other [127]. Another study only found improvement in a visuospatial organization task [128].…”

Section: Psychological and Neuropsychological Featuresmentioning

confidence: 92%

Persistent Comorbidities in Cushing’s Syndrome after Endocrine Cure

Resmini

2014

Advances in Endocrinology

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It was assumed that resolution of hypercortisolism in Cushing syndrome (CS) was followed by normalization of morbidity; however, in the last decade evidence is accumulating that patients with cured CS still have increased morbidity and mortality after the biochemical control of hypercortisolism. Patients with CS have an increased cardiovascular and metabolic risk and persistent accumulation of central fat, with an unfavorable adipokine profile, not only during the active phase of the disease but also long after biochemical remission. Clinical management should be particularly careful in identifying global cardiovascular risk, as a primary goal during the followup of these patients, aimed at improving global vascular morbidity. Moreover bone mass is reduced not only due to the endogenous hypercortisolism but also due to duration and dose of exogenous glucocorticoid (GC) replacement therapy after surgery. Thus, therapy in operated patients with inhibition of the hypothalamic-pituitary-adrenal axis should be reduced to the lowest dose and duration possible. Specific treatments should be considered in patients with decreased bone mass, aimed at reducing the increased fracture incidence. Finally, cognitive and health related quality of life impairments, described in active disease, are still abnormal after endocrine cure. Thus, residual morbidity persists in cured CS, suggesting irreversibility of GC-induced phenomena, typical of chronic hypercortisolism.

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“…Die beobachteten kortisoninduzierten kognitiven Störungen waren im Verlauf reversibel, persistierten jedoch gelegentlich bis zu mehreren Jahren [22]. Andererseits wurden bei Patienten mit pathologisch erhöhtem endogenen Kortisolspiegel (vornehmlich bei Morbus Cushing oder Depression) schwere kognitive Defizite beobachtet, v. a. des hippocampusabhän-gigen, deklarativen Gedächtnisses, aber auch solche, die andere Hirnregionen wie beispielsweise den präfrontalen Kortex, betreffen [5,10,13]. In Nachuntersuchungen wurden bei 13 operierten Cushing-Patienten 1 Jahr später weitgehend persistierende kognitive Defizite [6] festgestellt, hingegen ermittelten Starkman et al [16] nach 15,7 Monaten (±8,8 Monaten) bei 12 von 24 operierten Patienten neben verbesserten Gedächtnis-auch gesteigerte rechnerische Leistungen.…”

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Cognitive impairment after accidental high-dose corticosteroid therapy

et al. 2004

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Synthetic glucocorticosteroids can induce various severe mental disorders. Persisting cognitive disorder represents a rare complication of corticoid therapy involving memory, concentration, attention, or occupational performance. We observed the effects of a 20-day self-induced high-dose corticosteroid treatment on the cognitive functions in a 54-year-old patient. Having excluded dementia due to other organic causes, we examined the patient neuropsychologically immediately at the end of the steroid therapy and at follow-up (1, 2, 4, and 6 months). The initial tests showed seriously impaired functioning of concentration, attention, learning, and memory as well as of common ability to solve problems. The follow-up tests up to 6 months revealed an improvement of concentration and attention, but there were still serious deficits of the declarative memory with a high confabulating tendency. Our results confirm those of human experimental studies that exogenous steroids can cause serious persisting specific cognitive disorders especially of the declarative, hippocampus-dependent memory.

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The brain as a target for adrenocortical steroids: Cognitive implications

Cited by 123 publications

References 47 publications

MECHANISMS IN ENDOCRINOLOGY: Cushing's syndrome causes irreversible effects on the human brain: a systematic review of structural and functional magnetic resonance imaging studies

MECHANISMS IN ENDOCRINOLOGY: Cushing's syndrome causes irreversible effects on the human brain: a systematic review of structural and functional magnetic resonance imaging studies

Persistent Comorbidities in Cushing’s Syndrome after Endocrine Cure

Cognitive impairment after accidental high-dose corticosteroid therapy

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