scholarly journals Intranasal Insulin Administration to Prevent Delayed Neurocognitive Recovery and Postoperative Neurocognitive Disorder: A Narrative Review

Author(s):  
Rafael Badenes ◽  
Ega Qeva ◽  
Giovanni Giordano ◽  
Nekane Romero-García ◽  
Federico Bilotta

Delayed neurocognitive recovery and postoperative neurocognitive disorders are major complications of surgery, hospitalization, and anesthesia that are receiving increasing attention. Their incidence is reported to be 10–80% after cardiac surgery and 10–26% after non-cardiac surgery. Some of the risk factors include advanced age, level of education, history of diabetes mellitus, malnutrition, perioperative hyperglycemia, depth of anesthesia, blood pressure fluctuation during surgery, chronic respiratory diseases, etc. Scientific evidence suggests a causal association between anesthesia and delayed neurocognitive recovery or postoperative neurocognitive disorders, and various pathophysiological mechanisms have been proposed: mitochondrial dysfunction, neuroinflammation, increase in tau protein phosphorylation, accumulation of amyloid-β protein, etc. Insulin receptors in the central nervous system have a non-metabolic role and act through a neuromodulator-like action, while an interaction between anesthetics and central nervous system insulin receptors might contribute to anesthesia-induced delayed neurocognitive recovery or postoperative neurocognitive disorders. Acute or chronic intranasal insulin administration, which has no influence on the blood glucose concentration, appears to improve working memory, verbal fluency, attention, recognition of objects, etc., in animal models, cognitively healthy humans, and memory-impaired patients by restoring the insulin receptor signaling pathway, attenuating anesthesia-induced tau protein hyperphosphorylation, etc. The aim of this review is to report preclinical and clinical evidence of the implication of intranasal insulin for preventing changes in the brain molecular pattern and/or neurobehavioral impairment, which influence anesthesia-induced delayed neurocognitive recovery or postoperative neurocognitive disorders.

1993 ◽  
Vol 3 (3) ◽  
pp. 308-316 ◽  
Author(s):  
Gil Wernovsky ◽  
Richard A. Jonas ◽  
Paul R. Hickey ◽  
Adré J. du Plessis ◽  
Jane W. Newburger

The dramatic reduction in surgical mortality associated with repair of congenital heart anomalies in recent decades has been accompanied by a growing recognition of adverse neurologic sequels in some of the survivors. Abnormalities of the central nervous system may be a function of coexisting cerebral abnormalities or acquired events unrelated to surgical management (such as paradoxical embolus, cerebral infection, or effects of chronic cyanosis), but insults to the central nervous system appear to occur most frequently during or immediately after surgery. In particular, techniques of support used during neonatal and infant cardiac surgery—cardiopulmonary bypass, profound hypothermia and circulatory arrest—have been implicated as important causes of cerebral injury. This paper will review the effects of bypass and deep hypothermic circulatory arrest on neurodevelopmental outcome.


Nature ◽  
1978 ◽  
Vol 272 (5656) ◽  
pp. 827-829 ◽  
Author(s):  
JANA HAVRANKOVA ◽  
JESSE ROTH ◽  
MICHAEL BROWNSTEIN

2015 ◽  
Vol 47 (3) ◽  
pp. 715-728 ◽  
Author(s):  
Therese S. Salameh ◽  
Kristin M. Bullock ◽  
Isabel A Hujoel ◽  
Michael L. Niehoff ◽  
Tami Wolden-Hanson ◽  
...  

1990 ◽  
Vol 123 (1) ◽  
pp. 100-107
Author(s):  
L. Goya ◽  
C. Aláez ◽  
A. M. Pascual-Leone

Abstract. The development of epinephrine, norephinephrine, and total catecholamine secretion in plasma and andrenal glands was studied in newborn rats at short intervals: at day 2, 4, 6, 8, 10, 12 and 23. The increase in the plasma level of epinephrine represents a maturation of the secretion of the adrenal medulla. The increase in plasma of epinephrine and norepinephrine and the content of catecholamines in the adrenal glands of both normal animals and those treated with either high doses of T4 or cortisol at birth suggest a slowing down of the normal development of epinephrine secretion. This was confirmed by inducing hypoglycemia in these three groups of animals by a 20-h fast or by insulin administration (0.1436 μmol/kg). We conclude that both high doses of T4 and cortisol administered at birth seem to retard the development of the autonomic nervous system similar to the effect on the central nervous system.


10.1038/78682 ◽  
2000 ◽  
Vol 6 (8) ◽  
pp. 916-919 ◽  
Author(s):  
Frédérique Bard ◽  
Catherine Cannon ◽  
Robin Barbour ◽  
Rae-Lyn Burke ◽  
Dora Games ◽  
...  

2013 ◽  
Vol 4 (2) ◽  
pp. 86-89 ◽  
Author(s):  
Makoto Ishii ◽  
Ehud Lavi ◽  
Hooman Kamel ◽  
Ajay Gupta ◽  
Costantino Iadecola ◽  
...  

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