Hypoglycemia and its effect on the brain

Loose, Natara L.; Rudloff, Elke; Kirby, Rebecca

doi:10.1111/j.1476-4431.2008.00308.x

Cited by 16 publications

(16 citation statements)

References 80 publications

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“…When a hypoglycaemic event is not identified, the animal may experience seizure, critical brain damage, coma, and even death (Loose et al 2008). Although many incidences of unrecognised hypoglycaemia occur in veterinary medicine, the cause of the neurological signs associated with hypoglycaemia is not clear.…”

Section: Discussionmentioning

confidence: 98%

Comparison of continuous and intermittent glucose monitoring systems in a dog with diabetic ketoacidosis: a case report

Kim¹,

Kim²,

Kang³

et al. 2017

Vet. Med. - Czech

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ABSTRACT:A Miniature schnauzer (12 years old, neutered male) was referred for lethargy, anorexia, and oral bleeding. On initial evaluation, severe hyperglycaemia (blood glucose concentration of 34.9 mmol/l), ketonuria, systemic inflammation (fever, panting, left-shift neutrophilia, and a high C-reactive protein level of 980.97 nmol/l, abnormal pancreatic lipase immunoreactivity, and periodontitis were found. With consideration of possible insulin resistance, blood glucose (BG) levels were monitored using a portable glucose meter (q 1-3 h) and a continuous glucose monitoring system (CGMS) for 72 h (three consecutive trials); intensive insulin therapy was initiated using regular insulin (2.2 IU/kg intravenously). The insulin doses needed, based on the nadir, peak, and duration of insulin action from a traditional intermittent glucose curve were higher than those based on the CGMS results. Meanwhile, transient hyperglycaemic and hypoglycaemic periods, occurring between the intermittent measurements, were easily identified with the CGMS. Therefore, insulin resistance and the Somogyi phenomenon are less likely to occur with use of the CGMS than with intermittent BG measurements. By comparing data from a CGMS to those from an intermittent portable BG measurement system, this case report emphasises the importance and usefulness of a CGMS.

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Section: Discussionmentioning

confidence: 98%

Comparison of continuous and intermittent glucose monitoring systems in a dog with diabetic ketoacidosis: a case report

Kim¹,

Kim²,

Kang³

et al. 2017

Vet. Med. - Czech

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“…Oxygen is essential for aerobic energy production via oxidative phosphorylation; with oxygen deprivation, cell membrane ion pumps fail resulting in cell swelling (Calvert and Zhang 2005). Moreover, glucose deprivation may contribute to the development of neonatal encephalopathy as the brain consumes approximately 25% of total body glucose and thus depends on a constant supply of glucose to maintain homeostasis (Loose et al 2008). Other pathological processes that can contribute to the development of neonatal encephalopathy in infants include reperfusion injury (associated with oxidative injury), excitotoxicity (associated with excessive excitatory neurotransmitters such as glutamate), accumulation of intracellular calcium (associated with activation of numerous enzymes and pathways), increased inflammatory cytokines within the CNS (associated with altered neuronal and microglial function resulting in brain injury and cytotoxic oedema) and altered neuroactive steroid concentrations (associated with fetal/neonatal somnolence) (Mishra et al 2001;Calvert and Zhang 2005;Chew et al 2006;Kumar et al 2008;Loose et al 2008;Dickey et al 2011;Madigan et al 2012;Aleman et al 2013;Diesch and Mellor 2013).…”

Section: Discussionmentioning

confidence: 99%

Magnetic resonance imaging of presumptive neonatal encephalopathy in a foal

Wong

Jeffery

Hepworth-Warren

et al. 2016

Equine Veterinary Education

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Summary A 10‐h‐old Thoroughbred foal presented with clinical signs consistent with neonatal encephalopathy including absent suckling behaviour, lack of affinity for the mare and seizures. The foal was provided supportive care and treated with broad‐spectrum antimicrobials and fed via naso‐oesophageal tube. In addition, magnetic resonance imaging (MRI) was performed to investigate for structural changes that might be evident with equine neonatal encephalopathy. Notable findings on MRI included hyperintensity of the basal nuclei and superficial layers of the ventral cerebral hemispheres as well as the ventral thalamic nuclei and rostral aspect of the ventral midbrain. These imaging changes were consistent with the counterpart disease in infants and are the first to document MRI changes in a foal with neonatal encephalopathy. This report serves as an initial description of MRI findings associated with the presumed diagnosis of equine neonatal encephalopathy and also serves to solicit future diagnostic imaging studies that may help elucidate the pathophysiology and prognosis of equine neonatal encephalopathy.

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“…In hypoglycemic status, neuronal energy failure resulted in release of excitatory neurotransmitters (glutamate and aspartate), leading to calcium entry into the intracellular space and finally inducing neuronal apoptosis. 17 Therefore, low extracellular calcium concentrations might reduce the abnormal calcium influx and prevent neuronal death, and low serum calcium levels might thus have a protective role in HE. Notably, calcium signaling pathways play a crucial role in the survival of neurons.…”

Section: Discussionmentioning

confidence: 99%