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Hyperinsulinemia | definition of hyperinsulinemia by Medical dictionary
https://medical-dictionary.thefreedictionary.com/hyperinsulinemia
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hy·per·in·su·lin·ism

Increased levels of insulin in the plasma due to increased secretion of insulin by the beta cells of the pancreatic islets; decreased hepatic removal of insulin is a cause in some patients, although hyperinsulinism usually is associated with insulin resistance and is commonly found in obesity in association with varying degrees of hyperglycemia.
Farlex Partner Medical Dictionary © Farlex 2012
Excessive insulin in the blood.
Excessive insulin in the blood. Also called .
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by clearance 2014 new professional for sale Bella Toes Tan Casual Shoes zFd840
. All rights reserved.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.
Increased levels of insulin in the plasma due to increased secretion of insulin by the beta cells of the pancreatic islets. Synonym(s): hyperinsulinism , big discount NIKE air Max 2015 Mens Running Trainers 698902 Sneakers Shoes Spritedeep Royal Blue/Blackvoltgreen Strk cheap sale limited edition discount ebay low price fee shipping sale online 7CAhp0i4
.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
The medical term for high levels of insulin in the blood.
Mentioned in: Insulin Resistance , Polycystic Ovary Syndrome
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.
Increased levels of insulin in the plasma due to increased secretion of insulin by the beta cells of the islets of Langerhans. Synonym(s): hyperinsulinism , hyperinsulinaemia .
Medical Dictionary for the Dental Professions © Farlex 2012
a state of elevated levels of insulin in the body due to an improper dose of synthetic insulin or a result of an insulin-secreting tumor. Symptoms include excessive hunger, shakiness, and hypoglycemia.
Mosby's Dental Dictionary, 2nd edition. © 2008 Elsevier, Inc. All rights reserved.

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Size and Location

The 2 inherently appealing and most widely accepted explanations for the silence of SBI relate to the size and location of damaged brain tissue. As discussed above, SBIs predominantly involve small vessels and, consequently, are typically of limited size. It has been hypothesized that, because these infarcts are small, any associated neurological deficits remain covert. Similarly, the location of infarction is almost certainly of significance because large amounts of nonstrategic tissue can be lost without deficit, whereas small infarcts in vital areas (for example, in the brain stem and internal capsule) often have profound neurological sequelae. This speculation is supported by the predisposition for SBI to occur in certain locations. For instance, with lacunar infarcts, asymptomatic lesions typically occur in the vascular territory of the lenticulostriate penetrator arteries, whereas symptomatic lesions are predominantly located in the territory of the anterior choroidal artery. Interestingly, a higher proportion of posterior circulation and cerebellar SBI has been noted in younger patient cohorts and those having migraines. However, this pattern is also evident when examining the locations of overt strokes in younger cohorts.

Ischemic Preconditioning

Ischemic preconditioning is an innate adaptive and neuroprotective response to a previous sublethal insult that induces an ischemia-tolerant phenotype and increases resistance to a second, potentially lethal insult. This occurs through genomic reprogramming, resulting in an increase in de novo protein synthesis, cellular memory and neuronal plasticity and, consequently, a blunted injurious response and improved recovery. Intracellular survival signals are likely to be important for this response, especially the transcriptional activator hypoxia-inducible factor, which upregulates genes involved in the synthesis of erythropoietin, angiogenesis, vasomotor control, cell survival, pH regulation, and energy metabolism. For this reason, it has been postulated that chronic ischemic preconditioning and tolerance may enhance the clinical outcomes associated with brain tissue ischemia and infarction. Indeed, this is supported by the coexistence of SBI and leukoaraiosis, where the latter has been hypothesized to result from incomplete ischemia secondary to small-vessel disease.

Numerous studies have been published comparing the health outcomes in individuals with SBI versus those without. Evidence is considerable that SBI adversely affects the risk and outcomes of subsequent stroke, as well as overall neurocognitive and neuropsychiatric function, and risk of mortality ( Figure 5 ).

Figure 5.

Consequences of silent brain infarction.

Stroke

Recent controlled studies have documented an increased risk of first stroke among those with SBI that is as high as 10% per year and 5-fold that of those without SBI. In the largest community-based prospective study addressing this issue, Bokura et al followed up 2684 neurologically healthy subjects with no history of stroke (mean age, 58±7 years at entry) who underwent health screening, including MRI, to document the presence or absence of lesions such as SBI and were then followed up for a mean of 6.3 years. The incidence rates for clinical stroke were significantly higher in those with baseline SBI than those without (odds ratio, 3.66; 95% confidence interval, 2.28–5.89).

SBI has also been associated with the occurrence of recurrent stroke among patients experiencing a first stroke. Putaala et al performed Cox regression analysis on 655 young (15–49 years old) stroke victims followed up for a mean of 8.7±3.8 years and discovered that multiple SBI independently raised the risk of recurrent ischemic stroke (odds ratio, 2.48; 95% confidence interval, 1.24–4.94), even when adjusted for age, sex, other risk factors, stroke pathogenesis, and leukoaraiosis.

Neurocognitive Dysfunction

A variety of neurocognitive associations has been noted in individuals with SBI, ranging from global deterioration in cognitive function to diminished capacities relating to more specific brain processes, such as memory, procedural speed, and language. The presence of SBI on imaging is associated with a 2- to 3-fold increased frequency of dementia, postulated to result from ongoing brain infarction. Furthermore, among populations with dementia, those with SBI were more impaired than those without in several cognitive domains, including language function, delayed recall, and semantic fluency. Other associations with SBI include cerebral atrophy visual field defects, slowed rapid repetitive fine movements, gait disturbance, altered heel-toe walking, falls, and impaired mobility. Not surprisingly, the effect of SBI on neurocognitive function seems to vary with location; for instance, in the Northern Manhattan Study, SBI in frontal regions affects cognitive flexibility, whereas deep infarcts were associated with psychomotor slowing.

Psychiatric Disorders

In addition, SBI has been identified with increased frequency in patients with a variety of psychiatric disorders. The prevalence of SBI in older adults (mean age, >60 years) with depression has been found to be as high as 40% to 50%. In addition, SBI has been identified in 65% of bipolar patients whose psychosis started after the age of 50 years versus just 25% in those whose symptoms started earlier (<0.05), possibly suggesting a different mechanism of disease causation in the 2 age groups. There are several limitations of these results, including failure to control for other comorbid conditions, the small clinical-based (rather than community-based) and nonrandomly selected populations, and cross-sectional data collection that does not allow for inferences about causation. Nonetheless, these results certainly warrant further investigation.

Other Adverse Health Outcomes

Numerous other adverse health outcomes have been associated with an increased rate of SBI. The odds of pneumonia among seniors with SBI (mean age, 79 years) are almost 5-fold that of controls (odds ratio, 4.67; 95% confidence interval, 1.9–11.7). In addition, Willey et al looked at overall level of health and activity among 1238 clinically stroke-free adults recruited as part of the Northern Manhattan Study (mean age, 70±9 years) and discovered that the level of activity was poorer among those with SBI than those without, however, whether reduced activity arose secondary to SBI, or vice versa cannot be inferred.

Mortality

Finally, increased mortality has been documented in all studies on SBI that have addressed this issue. Of particular note are 2 large longitudinal community studies, in which the odds of death were increased 3- to 4-fold among those with SBI versus those without.

Conclusions

To date, studies have been plagued by inconsistencies in definitions and methodologies, limiting our current understanding of the phenomenon known as SBI. It is clear, however, that SBI is not rare and can no longer be considered as an incidental and clinically benign artifact on imaging scans. In fact, evidence strongly suggests that these lesions are frequently associated with neurocognitive, functional, and gait/mobility deficits that may be missed or attributed to other conditions, and that they predict the increased risk of more serious adverse neurological and cardiovascular events, including stroke and premature mortality. Much more is known about the risk factors for SBI than the underlying pathogenic mechanisms. Thus, understanding the former provides a useful platform for directed investigation of the latter. Although SBI share many associations with clinically overt strokes and transient ischemic attacks, differences clearly exist. As such, it may be overly simplistic to assume that entirely the same mechanisms give rise to all forms of cerebrovascular event. Here, we propose uniform criteria to standardize SBI definitions, which is necessary to facilitate homogeneity for future investigation.

Acknowledgments

We thank Drs White, Simpson, and Fanning for their assistance in preparation of the final article for submission.

Sources of Funding

Dr Fanning is funded by The Cardiac Society of Australia and New Zealand, The University of Queensland, The Prince Charles Hospital Foundation. Dr Fraser is funded by Office of Health and Medical Research Fellowship.

Disclosures

None.

Footnotes

The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.114.005919/-/DC1 .

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