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Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure. [22] Also, a life-threatening consequence of hyperglycemia can be nonketotic hyperosmolar syndrome. [16]
EDS can be considered as a broad condition encompassing several sleep disorders where increased sleep is a symptom, or as a symptom of another underlying disorder like narcolepsy, circadian rhythm sleep disorder, sleep apnea or idiopathic hypersomnia.
Sleep apnea is the second most frequent cause of secondary hypersomnia, affecting up to 4% of middle-aged adults, mostly men. Upper airway resistance syndrome (UARS) is a clinical variant of sleep apnea that can also cause hypersomnia. [8] Just as other sleep disorders (like narcolepsy) can coexist with sleep apnea, the same is true for UARS.
Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar non-ketotic state (HONK), is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. [4] [5] Symptoms include signs of dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness. [2]
Idiopathic hypersomnia (IH) is a neurological disorder which is characterized primarily by excessive sleep and excessive daytime sleepiness (EDS). [1] Idiopathic hypersomnia was first described by Bedrich Roth in 1976, and it can be divided into two forms: polysymptomatic and monosymptomatic.
Long-term complications from high blood sugar include heart disease, stroke, diabetic retinopathy, which can result in blindness, kidney failure, and poor blood flow in the lower-limbs, which may lead to amputations. [1] The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon. [4] [5]
Somnolence (alternatively sleepiness or drowsiness) is a state of strong desire for sleep, or sleeping for unusually long periods (compare hypersomnia). It has distinct meanings and causes. It has distinct meanings and causes.
To date, human studies have loosely examined the behavioral characteristics of postprandial sleep, demonstrating potential shifts in EEG spectra and self-reported sleepiness. [2] To date, the only clear animal models for examining the genetic and neuronal basis for this behavior are the fruit fly, the mouse, and the nematode Caenorhabditis elegans.