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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)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
According to an April 2010 U.S. Department of Veterans Affairs (VA) sponsored study conducted by the Institute of Medicine (IOM), part of the U.S. National Academy of Sciences, 250,000 of the 696,842 U.S. servicemen and women in the 1991 Gulf War continue to suffer from chronic multi-symptom illness, popularly known as "Gulf War Illness" or "Gulf War Syndrome." The IOM found that the chronic multi-symptom illness continues to affect these veterans nearly 20 years after the war.
According to the IOM, "It is clear that a significant portion of the soldiers deployed to the Gulf War have experienced troubling constellations of symptoms that are difficult to categorize," said committee chair Stephen L. Hauser, professor and chair, department of neurology, University of California, San Francisco (UCSF). "Unfortunately, symptoms that cannot be easily quantified are sometimes incorrectly dismissed as insignificant and receive inadequate attention and funding by the medical and scientific establishment. Veterans who continue to suffer from these symptoms deserve the very best that modern science and medicine can offer to speed the development of effective treatments, cures, and—we hope—prevention. Our report suggests a path forward to accomplish this goal, and we believe that through a concerted national effort and rigorous scientific input, answers can be found."
Questions still exist regarding why certain veterans showed, and still show, medically unexplained symptoms while others did not, why symptoms are diverse in some and specific in others, and why combat exposure is not consistently linked to having or not having symptoms. The lack of data on veterans' pre-deployment and immediate post-deployment health status and lack of measurement and monitoring of the various substances to which veterans may have been exposed make it difficult—and in many cases impossible—to reconstruct what happened to service members during their deployments nearly 20 years after the fact, the committee noted. The report called for a substantial commitment to improving identification and treatment of multisymptom illness in Gulf War veterans focussing on continued monitoring of Gulf War veterans, improved medical care, examination of genetic differences between symptomatic and asymptomatic groups and studies of environment-gene interactions.
A variety of signs and symptoms have been associated with GWS:
Birth defects have been suggested as a consequence of Gulf War deployment. However, a 2006 review of several studies of international coalition veterans' children found no strong or consistent evidence of an increase in birth defects, finding a modest increase in birth defects that was within the range of the general population, in addition to being unable to exclude recall bias as an explanation for the results. A 2008 report stated that "it is difficult to draw firm conclusions related to birth defects and pregnancy outcomes in Gulf War veterans", observing that while there have been "significant, but modest, excess rates of birth defects in children of Gulf War veterans", the "overall rates are still within the normal range found in the general population". The same report called for more research on the issue.
Medical ailments associated with Gulf War syndrome have been recognized by both the Department of Defense and the Department of Veterans Affairs. Since so little concrete information was known about this condition the Veterans Health Administration (VHA) originally classified individuals with related ailments believed to be connected to their service in the Persian Gulf a special non-ICD-9 code DX111, as well as ICD-9 code V65.5. There is no formal definition of the term "Gulf War syndrome" or "Gulf War illnesses".
Combat stress reaction symptoms align with the symptoms also found in psychological trauma, which is closely related to post-traumatic stress disorder (PTSD). CSR differs from PTSD (among other things) in that a PTSD diagnosis requires a duration of symptoms over one month, which CSR does not.
The most common stress reactions include:
- The slowing of reaction time
- Slowness of thought
- Difficulty prioritizing tasks
- Difficulty initiating routine tasks
- Preoccupation with minor issues and familiar tasks
- Indecision and lack of concentration
- Loss of initiative with fatigue
- Exhaustion
Shell shock is a phrase coined in World War I to describe the type of posttraumatic stress disorder many soldiers were afflicted with during the war (before PTSD itself was a term).
It is reaction to the intensity of the bombardment and fighting that produced a helplessness appearing variously as panic and being scared, or flight, an inability to reason, sleep, walk or talk.
During the War, the concept of shell shock was ill-defined. Cases of 'shell shock' could be interpreted as either a physical or psychological injury, or simply as a lack of moral fibre. The term "shell shock" is still used by the Veterans Administration to describe certain parts of PTSD but mostly it has entered into popular imagination and memory, and is often identified as the signature injury of the War.
In World War II and thereafter, diagnosis of 'shell shock' was replaced by that of combat stress reaction, a similar but not identical response to the trauma of warfare and bombardment.
During the early stages of World War I, soldiers from the British Expeditionary Force began to report medical symptoms after combat, including tinnitus, amnesia, headaches, dizziness, tremors, and hypersensitivity to noise. While these symptoms resembled those that would be expected after a physical wound to the brain, many of those reporting sick showed no signs of head wounds. By December 1914 as many as 10% of British officers and 4% of enlisted men were suffering from "nervous and mental shock".
The term "shell shock" came into use to reflect an assumed link between the symptoms and the effects of explosions from artillery shells. The term was first published in 1915 in an article in "The Lancet" by Charles Myers. Some 60–80% of shell shock cases displayed acute neurasthenia, while 10% displayed what would now be termed symptoms of conversion disorder, including mutism and fugue.
The number of shell shock cases grew during 1915 and 1916 but it remained poorly understood medically and psychologically. Some doctors held the view that it was a result of hidden physical damage to the brain, with the shock waves from bursting shells creating a cerebral lesion that caused the symptoms and could potentially prove fatal. Another explanation was that shell shock resulted from poisoning by the carbon monoxide formed by explosions.
At the same time an alternative view developed describing shell shock as an emotional, rather than a physical, injury. Evidence for this point of view was provided by the fact that an increasing proportion of men suffering shell shock symptoms had not been exposed to artillery fire. Since the symptoms appeared in men who had no proximity to an exploding shell, the physical explanation was clearly unsatisfactory.
In spite of this evidence, the British Army continued to try to differentiate those whose symptoms followed explosive exposure from others. In 1915 the British Army in France was instructed that:
However, it often proved difficult to identify which cases were which, as the information on whether a casualty had been close to a shell explosion or not was rarely provided.
Human exposure to bioaerosols has been documented to give rise to a variety of adverse health effects. Building occupants complain of symptoms such as sensory irritation of the eyes, nose, or throat; neurotoxic or general health problems; skin irritation; nonspecific hypersensitivity reactions; infectious diseases; and odor and taste sensations. Exposure to poor lighting conditions has led to general malaise.
Extrinsic allergic alveolitis has been associated with the presence of fungi and bacteria in the moist air of residential houses and commercial offices. A very large 2017 Swedish study correlated several inflammatory diseases of the respiration tract with objective evidence of damp-caused damage in homes.
The WHO has classified the reported symptoms into broad categories, including: mucous membrane irritation (eye, nose, and throat irritation), neurotoxic effects (headaches, fatigue, and irritability), asthma and asthma-like symptoms (chest tightness and wheezing), skin dryness and irritation, gastrointestinal complaints and more.
Several sick occupants may report individual symptoms which do not appear to be connected. The key to discovery is the increased incidence of illnesses in general with onset or exacerbation within a fairly close time frame—usually within a period of weeks. In most cases, SBS symptoms will be relieved soon after the occupants leave the particular room or zone. However, there can be lingering effects of various neurotoxins, which may not clear up when the occupant leaves the building. In some cases—particularly in sensitive individuals—there can be long-term health effects.
Mass psychogenic illness (MPI), also called mass sociogenic illness or just sociogenic illness, is "the rapid spread of illness signs and symptoms affecting members of a cohesive group, originating from a nervous system disturbance involving excitation, loss, or alteration of function, whereby physical complaints that are exhibited unconsciously have no corresponding organic" cause. MPI is distinct from other collective delusions, also included under the blanket terms of mass hysteria, in that MPI causes symptoms of disease, though there is no organic cause.
There is a clear preponderance of female victims. The DSM-IV-TR does not have specific diagnosis for this condition but the text describing conversion disorder states that "In 'epidemic hysteria', shared symptoms develop in a circumscribed group of people following 'exposure' to a common precipitant."
Qualities of MPI outbreaks often include:
- symptoms that have no plausible organic basis;
- symptoms that are transient and benign;
- symptoms with rapid onset and recovery;
- occurrence in a segregated group;
- the presence of extraordinary anxiety;
- symptoms that are spread via sight, sound or oral communication;
- a spread that moves down the age scale, beginning with older or higher-status people;
- a preponderance of female participants
Also, the illness may recur after the initial outbreak.
Symptoms range in severity from mild to disabling.
Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.
A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic and/or anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth, dry eyes, and an overactive bladder.
Multiple chemical sensitivity (MCS), also known as idiopathic environmental intolerances (IEI), is a disputed chronic condition characterized by symptoms that the affected person attributes to low-level exposures to commonly used chemicals. Symptoms are typically vague and non-specific. They may include fatigue, headaches, nausea, and dizziness.
Commonly attributed substances include scented products, pesticides, plastics, synthetic fabrics, smoke, petroleum products, and paint fumes.
Although the symptoms themselves are real, and can be disabling, MCS is not recognized as an organic, chemical-caused illness by the World Health Organization, American Medical Association, or any of several other professional medical organizations. Blinded clinical trials show that people with MCS react as often and as strongly to placebos as they do to chemical stimuli; the existence and severity of symptoms is related to perception that a chemical stimulus is present. Some attribute the symptoms to depression, somatoform disorders, or anxiety disorders.
Sick building syndrome (SBS) is a medical condition where people in a building suffer from symptoms of illness or feel unwell for no apparent reason. The symptoms tend to increase in severity with the time people spend in the building, and improve over time or even disappear when people are away from the building. The main identifying observation is an increased incidence of complaints of symptoms such as headache, eye, nose, and throat irritation, fatigue, and dizziness and nausea. These symptoms appear to be linked to time spent in a building, though no specific illness or cause can be identified. SBS is also used interchangeably with "building-related symptoms", which orients the name of the condition around patients rather than a "sick" building. A 1984 World Health Organization (WHO) report suggested up to 30% of new and remodeled buildings worldwide may be subject of complaints related to poor indoor air quality.
Sick building causes are frequently pinned down to flaws in the heating, ventilation, and air conditioning (HVAC) systems. However, there have been inconsistent findings on whether air conditioning systems result in SBS or not. Other causes have been attributed to contaminants produced by outgassing of some types of building materials, volatile organic compounds (VOC), molds (see mold health issues), improper exhaust ventilation of ozone (byproduct of some office machinery), light industrial chemicals used within, or lack of adequate fresh-air intake/air filtration (see Minimum efficiency reporting value).
The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.
Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.
The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.
The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.
Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.
Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity. Symptoms include miosis, sweating, lacrimation, gastrointestinal symptoms, respiratory difficulties, shortness of breath, slowed heart rate, cyanosis, vomiting, diarrhea, trouble sleeping, as well as other symptoms. Along with these central effects can be seen and finally seizures, convulsions, coma, respiratory failure. If the person survives the first day of poisoning personality changes can occur, aggressive events, psychotic episodes, disturbances and deficits in memory and attention, as well as other delayed effects. When death occurs, it is most commonly due to respiratory failure from the combination of central and peripheral effects, paralysis of respiratory muscles and depression of the brain respiratory center. For people afflicted with cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning. Diazepam is sometimes also administered in combination with the atropine and oximes.
The intermediate syndrome (IMS) appears in the interval between the end of the cholinergic crisis and the onset of OPIDP. Symptoms associated with IMS manifest within 24–96 hours after exposure. The exact etiology, incidence, and risk factors associated with IMS are not clearly understood, but IMS is recognized as a disorder of neuromuscular junctions. IMS occurs when a person has a prolonged and severe inhibition of AChE and has been linked to specific OP pesticides such as methylparathion, dichlorvos, and parathion. Patients present with increasing weakness of facial, neck flexor and respiratory muscles.
OPIDP occurs in a small percentage of cases, roughly two weeks after exposure, where temporary paralysis occurs. This loss of function and ataxia of peripheral nerves and spinal cord is the phenomenon of OPIDP. Once the symptoms begin with shooting pains in both legs, the symptoms continue to worsen for 3–6 months. In the most severe cases quadriplegia has been observed. Treatment only affects sensory nerves, not motor neurons which may permanently lose function. The aging and phosphorylation of more than 70% of functional NTE in peripheral nerves is one of the processes involved in OPIDP. Standard treatments for OP poisoning are ineffective for OPIDP.
COPIND occurs without cholinergic symptoms and is not dependent on AChE inhibition. COPIND appears with a delay and is long lasting. Symptoms associated with COPIND include cognitive deficit, mood change, autonomic dysfunction, peripheral neuropathy, and extrapyramidal symptoms. The underlying mechanisms of COPIND have not been determined, but it is hypothesized that withdrawal of OP pesticides after chronic exposure or acute exposure could be a factor.
A self-inflicted wound (SIW), is the act of harming oneself where there are no underlying psychological problems related to the self-injury, but where the injurer wanted to take advantage of being injured.
Symptoms of PTSD generally begin within the first 3 months after the inciting traumatic event, but may not begin until years later. In the typical case, the individual with PTSD persistently avoids trauma-related thoughts and emotions, and discussion of the traumatic event, and may even have amnesia of the event. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares. While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder).
Anti-Chinese sentiment in Japan has been present since the Tokugawa period. Anti-Chinese sentiments in Japan have been on a sharp rise since 2002. According to Pew Global Attitude Project (2008), unfavorable view of China was 84%, unfavorable view of Chinese people was 73%.
Viet Nguyen (, February 25, 1981 – October 6, 2007) and Duc Nguyen (, born February 25, 1981) were a pair of conjoined twins born in Vietnam and surgically separated in 1988. Viet died in 2007 of natural causes.
Viet and Duc were born on February 25, 1981, in Kon Tum Province, Tây Nguyên, Vietnam. Viet was the elder and Duc was the younger of the two brothers. Their relatives claim that "the reason they became conjoined twins is the influence of Agent Orange that the U.S. military used as a defoliant during the Vietnam War". His mother was farming in the area doused with Agent Orange a year after the Vietnam War had ended. She also drank water from a well in that area. After that, Viet and Duc were born. On October 4, 1988, Viet and Duc were separated in the hospital in Ho Chi Minh City with the help of the Japanese Red Cross after Viet went into a coma.
Duc first entered junior high school, then dropped out and learned computer programming in a school. Now, he works at a hospital in Ho Chi Minh City. On December 16, 2006, he married Nguyen Thanh Tuyen in Ho Chi Minh City.
Viet's health problems continued after the separation, and he died due to liver failure and pneumonia on October 6, 2007, at the age of 26.
Cyberchondria, otherwise known as 'compucondria', is the unfounded escalation of concerns about common symptomology based on review of search results and literature online. Articles in popular media position cyberchondria anywhere from temporary neurotic excess to adjunct hypochondria. Cyberchondria is a growing concern among many healthcare practitioners as patients can now research any and all symptoms of a rare disease, illness or condition, and manifest a state of medical anxiety.
Gueules cassées (broken faces) is a French expression for facially disfigured servicemen which originated in World War I. Colonel Yves Picot is said to have coined the term when he was refused passing a checkpoint to a party.
Posttraumatic stress disorder (PTSD) is a mental disorder that can develop after a person is exposed to a traumatic event, such as sexual assault, warfare, traffic collisions, or other threats on a person's life. Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in how a person thinks and feels, and an increase in the fight-or-flight response. These symptoms last for more than a month after the event. Young children are less likely to show distress but instead may express their memories through play. A person with PTSD is at a higher risk for suicide and intentional self-harm.
Most people who have experienced a traumatic event will not develop PTSD. People who experience interpersonal trauma (for example rape or child abuse) are more likely to develop PTSD, as compared to people who experience non-assault based trauma such as accidents and natural disasters. About half of people develop PTSD following rape. Children are less likely than adults to develop PTSD after trauma, especially if they are under ten years of age. Diagnosis is based on the presence of specific symptoms following a traumatic event.
Prevention may be possible when therapy is targeted at those with early symptoms but is not effective when carried out among all people following trauma. The main treatments for people with PTSD are counselling and medication. A number of different types of therapy may be useful. This may occur one-on-one or in a group. Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people. These benefits are less than those seen with therapy. It is unclear if using medications and therapy together has greater benefit. Other medications do not have enough evidence to support their use and in the case of benzodiazepines may worsen outcomes.
In the United States about 3.5% of adults have PTSD in a given year, and 9% of people develop it at some point in their life. In much of the rest of the world, rates during a given year are between 0.5% and 1%. Higher rates may occur in regions of armed conflict. It is more common in women than men. Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks. During the World Wars study increased and it was known under various terms including "shell shock" and "combat neurosis". The term "posttraumatic stress disorder" came into use in the 1970s in large part due to the diagnoses of U.S. military veterans of the Vietnam War. It was officially recognized by the American Psychiatric Association in 1980 in the third edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-III).
Radiophobia is an obsessive fear of ionizing radiation, in particular, fear of X-rays. While in some cases radiation may be harmful (i.e. radiation-induced cancer, and acute radiation syndrome), the effects of poor information, understanding, or a traumatic experience may cause unnecessary or even irrational fear. The term is also used in a non-medical sense to describe the opposition to the use of nuclear technology (i.e. nuclear power) arising from concerns disproportionately greater than actual risks would merit.
Da Costa's syndrome is generally considered a physical manifestation of an anxiety disorder.
One of the main effects of cadmium poisoning is weak and brittle bones. Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the cadmium. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Other complications include coughing, anemia, and kidney failure, leading to death.
A marked prevalence in older, postmenopausal women has been observed. The cause of this phenomenon is not fully understood, and is currently under investigation. Current research has pointed to general malnourishment, as well as poor calcium metabolism relating to the women's age.
Recent animal studies have shown that cadmium poisoning alone is not enough to elicit all of the symptoms of itai-itai disease. These studies are pointing to damage of the mitochondria of kidney cells by cadmium as a key factor of the disease.
Viliuisk Encephalomyelitis (VE) is a fatal progressive neurological disorder found only in the Sakha (Iakut/Yakut) population of central Siberia. About 15 new cases are reported each year. VE is a very rare disease and little research has been conducted. The causative agents, origin of the disease, and involved candidate genes are currently unknown, but much research has been done in pursuit of the answers.
Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma. In all cases the disease is fatal.