Effects of neonatal hypoglycaemia on the nervous system: a pathological study.

Anderson, J.; Milner, R. D. G.; Strich, SabinaJ.

doi:10.1136/jnnp.30.4.295

Cited by 174 publications

(58 citation statements)

References 39 publications

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“…50 The findings are in keeping with pathological studies that show widespread injury after prolonged and severe hypoglycaemia, 36,37,51 and suggest that posterior white matter and cortex may not be as selectively vulnerable as suggested previously.…”

Section: Magnetic Resonance Imagingsupporting

confidence: 84%

“…24,34,35 The spectrum of injury associated with hypoglycaemia is reported to be wide and includes parenchymal haemorrhage, ischaemic stroke, cortical neuronal injury, corticospinal tract injury, and signal intensity changes in the basal ganglia and thalami on MRI. [36][37][38][39][40][41][42][43][44][45][46][47][48] A regional vulnerability of the white matter and cortex of the parietal and occipital lobes is described (Fig. 1b).…”

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

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Hypoglycaemia and hypoxic–ischaemic encephalopathy

Boardman

Hawdon

2015

Develop Med Child Neuro

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HIE Hypoxic-ischaemic encephalopathyThe transition from fetal to neonatal life requires metabolic adaptation to ensure that energy supply to vital organs and systems is maintained after separation from the placental circulation. Under normal conditions, this is achieved through the mobilization and use of alternative cerebral fuels (fatty acids, ketone bodies, and lactate) when blood glucose concentration falls. Severe hypoxia-ischaemia is associated with impaired metabolic adaptation, and animal and human data suggest that levels of hypoglycaemia that are tolerated under normal conditions can be harmful in association with hypoxia-ischaemia. The optimal target blood glucose level for ensuring adequate energy provision in hypoxic-ischaemic encephalopathy (HIE) remains unknown. However, recent data support guidance to maintain a blood glucose concentration of 2.5mmol/L or more in neonates with signs of acute neurological dysfunction, which includes those with HIE, and this is higher than the accepted threshold of 2mmol/L in infants without signs of neurological dysfunction or hyperinsulinism. CEREBRAL ENERGY SUFFICIENCY AND METABOLIC ADAPTATION AT BIRTHDuring fetal life, the predominant source of brain energy is glucose, which crosses the placenta by facilitated diffusion; there is very little endogenous glucose production under normal circumstances, although this increases in cases of intrauterine growth restriction and placental insufficiency. Ketone bodies and lactate may also be cerebral energy substrates in the healthy fetus. Amino acids, free fatty acids, and glycerol from the placental circulation are typically used for growth and the accumulation of fuel stores in preparation for birth, but they can serve as brain energy substrates if there is fetal growth restriction. 1,2During labour, the fetus is exposed to physiological challenges that require metabolic adaptation to occur if cerebral energy sufficiency is to be preserved. Anaerobic metabolism occurs under the transient hypoxic conditions of a typical labour, and this consumes more substrate than oxidative metabolism would. There is an abrupt cessation of continuous substrate supply when the placental circulation is divided, with a consequent drop in blood glucose concentration, and the fetus must then adapt to use lipids as the predominant energy substrate. A healthy infant successfully manages the postnatal transition by mobilizing and using alternative cerebral fuels including ketone bodies, fatty acids, and lactate. After birth, there is a rapid surge in catecholamine and glucagon levels, and a steady decrease in insulin, at the same time as blood glucose levels decline. These hormonal changes induce enzyme activities that lead to glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis, which, in turn, provide endogenous glucose, free fatty acids, and ketone bodies.2,3 These substrates, together with lactate, meet the energy requirements of the neonatal brain in most situations. In some circumstances, this metabolic adaptation can be predicted...

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Section: Magnetic Resonance Imagingsupporting

confidence: 84%

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Hypoglycaemia and hypoxic–ischaemic encephalopathy

Boardman

Hawdon

2015

Develop Med Child Neuro

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“…Similar topographical distribution of neuropathology was observed in premature infants using autopsy studies, computed tomography, magnetic resonance imaging and single photon emission computed tomography blood flow scans (Anderson et al, 1967;Spar et al, 1994;Chiu et al, 1998;Volpe, 2008). The hypoglycemic brain injury primarily involves neurons but glia are also affected (Anderson et al, 1967). Studies of oligodendrocyte precursor cells and cerebellar slice cultures showed that www.intechopen.com hypoglycemia induces apoptotic cell death and inhibits differentiation and myelination (Yan & Rivkees 2006).…”

Section: Pathological Changes In Hypoglycemic Brain Injurymentioning

confidence: 61%

“…The injury was most severe in regions contiguous to cerebrospinal fluid such as superficial cerebral cortical layers (Agardh et al, 1980;Auer et al, 1984Auer et al, , 1985Kalimo et al, 1985;Siesjo, 1988). Similar topographical distribution of neuropathology was observed in premature infants using autopsy studies, computed tomography, magnetic resonance imaging and single photon emission computed tomography blood flow scans (Anderson et al, 1967;Spar et al, 1994;Chiu et al, 1998;Volpe, 2008). The hypoglycemic brain injury primarily involves neurons but glia are also affected (Anderson et al, 1967).…”

Section: Pathological Changes In Hypoglycemic Brain Injurymentioning

confidence: 65%

An Update on Neonatal Hypoglycemia

Kumar¹,

Saini²

2011

Hypoglycemia - Causes and Occurrences

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“…[31][32][33] In one study there were radiological abnormalities in 94% of term neonates with hypoglycaemia (blood glucose levels < 2.6 mmol/l). 34,35 In 30 neonates exposed to a balanced salt solution with or without glucose, it was found that the blood glucose was low in the group given only a balanced salt solution if a preoperative glucose infusion was interrupted at the start of anaesthesia.…”

Section: Should Maintenance Fluid Contain Glucose?mentioning

confidence: 99%