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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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Among the causes of hypopnea are:
- anatomical defects such as nasal septum deformation or congenital narrowness of nasal meatus and the gullet
- acute tonsillitis and/or adenoiditis
- obesity or being overweight
- neuromuscular disease or any condition that entails weakened respiratory muscles
- hypoventilation syndromes involving compromised or failed respiratory drive
- use of sedatives e.g. sleeping pills
- alcohol abuse
- smoking
- aging
- others, most of which are also typical causes of airway obstruction, snoring and sleep apnea
Hypopnea is a disorder that may result in excessive daytime sleepiness and compromised quality of life, including traffic accidents, diminished productivity in the workplace, and emotional problems.
Cardiovascular consequences of hypopnea may include myocardial infarction, stroke, psychiatric problems, impotence, cognitive dysfunction, hypertension, coronary heart disease, and memory loss.
The conditions of hypoxia and hypercapnia, whether caused by apnea or not, trigger additional effects on the body. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures, how short is the interval between failures to breathe, and the presence or absence of independent conditions whose effects amplify those of an apneic episode.
- Brain cells need constant oxygen to live, and if the level of blood oxygen remains low enough for long enough, brain damage and even death will occur. These effects, however, are rarely a result of central sleep apnea, which is a chronic condition whose effects are usually much milder.
- Drops in blood oxygen levels that are severe but not severe enough to trigger brain-cell or overall death may trigger seizures even in the absence of epilepsy.
- In severe cases of sleep apnea, the more translucent areas of the body will show a bluish or dusky cast from cyanosis, the change in hue ("turning blue") produced by the deoxygenation of blood in vessels near the skin.
- Compounding effects of independent conditions:
Many studies indicate the effect of a "fight or flight" response on the body that happens with each apneic event is what increases health risks and consequences in OSA. The fight or flight response causes many hormonal changes in the body; those changes, coupled with the low oxygen saturation level of the blood, cause damage to the body over time.
Without treatment, the sleep deprivation and lack of oxygen caused by sleep apnea increases health risks such as cardiovascular disease, aortic disease (e.g. aortic aneurysm), high blood pressure, stroke, diabetes, clinical depression, weight gain and obesity.
The most serious consequence of untreated OSA is to the heart. Persons with sleep apnea have a 30% higher risk of heart attack or death than those unaffected. In severe and prolonged cases, increased in pulmonary pressures are transmitted to the right side of the heart. This can result in a severe form of congestive heart failure known as "cor pulmonale". Dyastolic function of the heart also becomes affected. One prospective study showed patients with OSA, compared with healthy controls, initially had statistically significant increases in vascular endothelial growth factor (P=.003) and significantly lower levels of nitrite-nitrate (P=.008), which might be pathogenic factors in the cardiovascular complications of OSA. These factors reversed to normal levels after 12 weeks of treatment by CPAP, but further long-term trials are needed to assess the impact of this therapy.
Elevated arterial pressure (i.e., hypertension) can be a consequence of OSA syndrome. When hypertension is caused by OSA, it is distinctive in that, unlike most cases (so-called essential hypertension), the readings do "not" drop significantly when the individual is sleeping (non-dipper) or even increase (inverted dipper).
Sleep apnea can affect people regardless of sex, race, or age. However, risk factors include:
- being male
- excessive weight
- an age above 40
- large neck size (greater than 16–17 inches)
- enlarged tonsils or tongue
- small jaw bone
- gastroesophageal reflux
- allergies
- sinus problems
- a family history of sleep apnea
- deviated septum
Alcohol, sedatives and tranquilizers may also promote sleep apnea by relaxing throat muscles. Smokers have sleep apnea at three times the rate of people who have never smoked.
Central sleep apnea is more often associated with any of the following risk factors:
- being male
- an age above 65
- having heart disorders such as atrial fibrillation or atrial septal defects such as PFO
- stroke
High blood pressure is very common in people with sleep apnea.
The Wisconsin Sleep Cohort Study estimated in 1993 that roughly one in every 15 Americans was affected by at least moderate sleep apnea. It also estimated that in middle-age as many as nine percent of women and 24 percent of men were affected, undiagnosed and untreated.
The costs of untreated sleep apnea reach further than just health issues. It is estimated that in the U.S. the average untreated sleep apnea patient's annual health care costs $1,336 more than an individual without sleep apnea. This may cause $3.4 billion/year in additional medical costs. Whether medical cost savings occur with treatment of sleep apnea remains to be determined.
Congenital central hypoventilation syndrome (CCHS), often referred to by its older name "Ondine's curse," is a rare and very severe inborn form of abnormal interruption and reduction in breathing during sleep. This condition involves a specific homeobox gene, PHOX2B, which guides maturation of the autonomic nervous system; certain loss-of-function mutations interfere with the brain's development of the ability to effectively control breathing. There may be a recognizable pattern of facial features among individuals affected with this syndrome.
Once almost uniformly fatal, CCHS is now treatable. Children who have it must have tracheotomies and access to mechanical ventilation on respirators while sleeping, but most do not need to use a respirator while awake. The use of a diaphragmatic pacemaker may offer an alternative for some patients. When pacemakers have enabled some children to sleep without the use of a mechanical respirator, reported cases still required the tracheotomy to remain in place because the vocal cords did not move apart with inhalation.
Persons with the syndrome who survive to adulthood are strongly instructed to avoid certain condition-aggravating factors, such as alcohol use, which can easily prove lethal.
OSA accompanied by daytime sleepiness is estimated to affect 3% to 7% of men and 2% to 5% of women, and the disease is common in both developed and developing countries. It is most commonly diagnosed in middle-aged males.
If studied carefully in a sleep lab by polysomnography (formal "sleep study"), it is believed that approximately 1 in 5 American adults would have at least mild OSA.
Obesity hypoventilation syndrome is associated with a reduced quality of life, and people with the condition incur increased healthcare costs, largely due to hospital admissions including observation and treatment on intensive care units. OHS often occurs together with several other disabling medical conditions, such as asthma (in 18–24%) and type 2 diabetes (in 30–32%). Its main complication of heart failure affects 21–32% of patients.
Those with abnormalities severe enough to warrant treatment have an increased risk of death reported to be 23% over 18 months and 46% over 50 months. This risk is reduced to less than 10% in those receiving treatment with PAP. Treatment also reduces the need for hospital admissions and reduces healthcare costs.
The exact prevalence of obesity hypoventilation syndrome is unknown, and it is thought that many people with symptoms of OHS have not been diagnosed. About a third of all people with morbid obesity (a body mass index exceeding 40 kg/m) have elevated carbon dioxide levels in the blood.
When examining groups of people with obstructive sleep apnea, researchers have found that 10–20% of them meet the criteria for OHS as well. The risk of OHS is much higher in those with more severe obesity, i.e. a body mass index (BMI) of 40 kg/m or higher. It is twice as common in men compared to women. The average age at diagnosis is 52. American Black people are more likely to be obese than American whites, and are therefore more likely to develop OHS, but obese Asians are more likely than people of other ethnicities to have OHS at a lower BMI as a result of physical characteristics.
It is anticipated that rates of OHS will rise as the prevalence of obesity rises. This may also explain why OHS is more commonly reported in the United States, where obesity is more common than in other countries.
According to one meta-analysis, the mean prevalence rate for North America and Western Europe is estimated to be 14.5±8.0%. Specifically in the United States, the prevalence of restless leg syndrome is estimated to be between 5 and 15.7% when using strict diagnostic criteria. RLS is over 35% more prevalent in American women than their male counterparts.
A systematic review states 7.6% of the general population experiences sleep paralysis at least once in their lifetime. Its prevalence among men is 15.9% while 18.9% of women experience it. When considering specific populations, 28.3% of students and 31.9% of psychiatric patients have experienced this phenomenon at least once in their lifetime. Of those psychiatric patients, 34.6% have panic disorder. Sleep paralysis in students is slightly more prevalent for those of Asian descent (39.9%) than other ethnicities (Hispanic: 34.5%, African descent: 31.4%, Caucasian 30.8%).
Sexsomnia affects individuals of all age groups and backgrounds but present as an increased risk for individuals who possess the following:
- coexisting sleep disorders
- sleep disruption secondary to obstructive sleep apnea
- sleep related epilepsy
- certain medications
Behaviors of pelvic thrusting, sexual arousal, and orgasms are often attributed to sleep related epilepsy disorder. In some cases, physical contact with a partner in bed acted as a trigger to initiate sexsomia behaviors.
Medications, such as the commonly prescribed treatment for insomnia, Ambien, have been shown to induce symptoms commonly associated with sexsomnia.
Like sleep-related eating disorders, sexsomnia presents more commonly in adults than children. However, these individuals usually have a history of parasomnias that began during childhood.
Symptoms of sexsomnia can be caused by or be associated with:
- stress factors
- sleep deprivation
- Consumption of alcohol or other drugs
- Pre-existing parasomnia behaviors
Sleep deprivation is known to have negative effects on the brain and behavior. Extended periods of sleep deprivation often results in the malfunctioning of neurons, directly effecting an individual's behavior. While muscles are able to regenerate even in the absence of sleep, neurons are incapable of this ability. Specific stages of sleep are responsible for the regeneration of neurons while others are responsible for the generation of new synaptic connections, the formation of new memories, etc.
Zolpidem, the widely known sedative Ambien, is used as common treatment for insomnia and has been seen to result in sexsomnia as an adverse effect.
Sexsomnia can also be triggered by physical contact initiated by a partner, or an individual sharing the same bed.
There are various individual risk factors associated with having a silent stroke. Many of these risk factors are the same as those associated with having a major symptomatic stroke.
- Acrolein: elevated levels of acrolein, a toxic metabolite produced from the polyamines spermine, spermidine and by amine oxidase serve as a marker for silent stroke, when elevated in conjunction with C-reactive protein and interleukin 6 the confidence levels in predicting a silent stroke risk increase.
- Adiponectin: is a type of protein secreted by adipose cells that improves insulin sensitivity and possesses antiatherogenic properties. Lower levels of s-adiponectin are associated with ischemic stroke.
- Aging: the prevalence of silent stroke rises with increasing age with a prevalence rate of over twenty percent of the elderly increasing to 30%-40% in those over the age of 70.
- Anemia: children with acute anemia caused by medical conditions other than sickle cell anemia with hemoglobin below 5.5 g/dL. are at increased risk for having a silent stroke according to a study released at American Stroke Association's International Stroke Conference 2011. The researchers suggested a thorough examination for evidence of silent stroke in all severely anemic children in order to facilitate timely intervention to ameliorate the potential brain damage.
- Sickle cell anemia: is an autosomal recessive genetic blood disorder caused in the gene (HBB gene) which codes for hemoglobin (Hg) and results in lowered levels. The blood cells in sickle cell disease are abnormally shaped (sickle-shaped) and may form clots or block blood vessels. Estimates of children with sickle cell anemia who suffer strokes (with silent strokes predominating in the younger patients) range from 15%-30%. These children are at significant risk of cognitive impairment and poor educational outcomes.
- Thalassemia major: is an autosomal recessive genetically inherited form of hemolytic anemia, characterized by red blood cell (hemoglobin) production abnormalities. Children with this disorder are at increased risk for silent stroke.
- Atrial fibrillation (AF): atrial fibrillation (irregular heartbeat) is associated with a doubled risk for silent stroke.
- Cigarette smoking: The procoagulant and atherogenic effects of smoking increase the risk for silent stroke. Smoking also has a deleterious effect on regional cerebral blood flow (rCBF). The chances of having a stroke increase with the amount of cigarettes smoked and the length of time an individual has smoked (pack years).
- C-reactive protein (CRP) and Interleukin 6 (IL6): C-reactive protein is one of the plasma proteins known as acute phase proteins (proteins whose plasma concentrations increase (or decrease) by 25% or more during inflammatory disorders) which is produced by the liver. The level of CRP rises in response to inflammation in various parts of the body including vascular inflammation. The level of CRP can rise as high as 1000-fold in response to inflammation. Other conditions that can cause marked changes in CRP levels include infection, trauma, surgery, burns, inflammatory conditions, and advanced cancer. Moderate changes can also occur after strenuous exercise, heatstroke, and childbirth. Increased levels of CRP as measured by a CRP test or the more sensitive high serum CRP (hsCRP) test have a close correlation to increased risk of silent stroke. Interleukin-6 is an interleukin (type of protein) produced by T-cells (specialized white blood cells), macrophages and endothelial cells. IL6 is also classified as a cytokine (acts in relaying information between cells). IL6 is involved in the regulation of the acute phase response to injury and infection may act as both an anti-inflammatory agent and a pro-inflammatory.Increased levels of CRP as measured by a CRP test or the more sensitive high serum CRP (hsCRP) test and elevated levels of I6 as measured by an IL6 ELISA are markers for the increased risk of silent stroke.
- Diabetes mellitus: untreated or improperly managed diabetes mellitus is associated with an increased risk for silent stroke.
- Hypertension: which affects up to 50 million people in the United States alone is the major treatable risk factor associated with silent stokes.
- Homocysteine: elevated levels of total homocysteine (tHcy) an amino acid are an independent risk factor for silent stroke, even in healthy middle-aged adults.
- Metabolic syndrome (MetS):Metabolic syndrome is a name for a group of risk factors that occur together and increase the risk for coronary artery disease, stroke, and type 2 diabetes. A higher number of these MetS risk factors the greater the chance of having a silent sroke.
- Polycystic ovary syndrome (PCOS): is associated with double the risk for arterial disease including silent stroke independent of the subjects Body mass index (BMI).
- Sleep apnea: is a term which encompasses a heterogeneous group of sleep-related breathing disorders in which there is repeated intermittent episodes of breathing cessation or hypopnea, when breathing is shallower or slower than normal. Sleep apnea is a common finding in stroke patients but recent research suggests that it is even more prevalent in silent stroke and chronic microvascular changes in the brain. In the study presented at the American Stroke Association's International Stroke Conference 2012 the higher the apnea-hypopnea index, the more likely patients had a silent stroke.
Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity, as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality.
The Great Imitator (also The Great Masquerader) is a phrase used for medical conditions that feature nonspecific symptoms and may be confused with a number of other diseases. Most great imitators are systemic in nature. Diseases sometimes referred to with this name include:
- Various cancers
- Intravascular large B-cell lymphoma
- Various rheumatic conditions, including:
- Fibromyalgia
- Psoriatic arthritis
- Lupus erythematosus
- Systemic lupus erythematosus
- Sarcoidosis
- Multiple sclerosis
- Celiac disease
- Addison's Disease
- Pulmonary embolism
- Various infectious diseases, including:
- Syphilis
- Lyme disease
- Nocardiosis
- Tuberculosis
- Brucellosis
- Malaria
- Breathing-related sleep disorders (chiefly sleep apnea/hypopnea and upper-airway resistance syndrome).
Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:
- Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.
- Injury to nerves caused by surgery or radiation to the neck.
- Treatment with certain medications, including some drugs used in cancer chemotherapy.
- Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.
- Other chronic illnesses, such as Parkinson's disease, multiple sclerosis and some types of dementia.
- Autonomic neuropathy may also be caused by an abnormal attack by the immune system that occurs as a result of some cancers (paraneoplastic syndrome).
- Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.
- Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.
- Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain-Barre syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.
The signs and symptoms of autonomic neuropathy include the following:
- Urinary bladder conditions: bladder incontinence or urinary retention
- Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation
- Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion
- Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).
- Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.
- Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).
Mononeuropathy is a type of neuropathy that only affects a single nerve. Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.
The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.
Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include systemic diseases (such as diabetes or leprosy), vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including Metronidazole and the fluoroquinolone class of antibiotics (Ciprofloxacin, Levaquin, Avelox etc.), traumatic injury, including ischemia, radiation therapy, excessive alcohol consumption, immune system disease, Coeliac disease, or viral infection. It can also be genetic (present from birth) or idiopathic (no known cause). In conventional medical usage, the word "neuropathy" (, "nervous system" and , "disease of") without modifier usually means "peripheral neuropathy".
Neuropathy affecting just one nerve is called "mononeuropathy" and neuropathy involving nerves in roughly the same areas on both sides of the body is called "symmetrical polyneuropathy" or simply "polyneuropathy". When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called "mononeuritis multiplex", "multifocal mononeuropathy", or "multiple mononeuropathy".mononeuritis multiplex
Peripheral neuropathy may be chronic (a long-term condition where symptoms begin subtly and progress slowly) or acute (sudden onset, rapid progress, and slow resolution). Acute neuropathies demand urgent diagnosis. Motor nerves (that control muscles), sensory nerves, or autonomic nerves (that control automatic functions such as heart rate, body temperature, and breathing) may be affected. More than one type of nerve may be affected at the same time. Peripheral neuropathies may be classified according to the type of nerve predominantly involved, or by the underlying cause.
Neuropathy may cause painful cramps, fasciculations (fine muscle twitching), muscle loss, bone degeneration, and changes in the skin, hair, and nails. Additionally, motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or skin allodynia (severe pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally.