<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chest pain and explain in detail? [/INST] Chest pain is pain or discomfort in the chest, typically the front of the chest. It may be described as sharp, dull, pressure, heaviness or squeezing. Associated symptoms may include pain in the shoulder, arm, upper abdomen, or jaw, along with nausea, sweating, or shortness of breath. It can be divided into heart-related and non-heart-related pain. Pain due to insufficient blood flow to the heart is also called angina pectoris. Those with diabetes or the elderly may have less clear symptoms.Serious and relatively common causes include acute coronary syndrome such as a heart attack (31%), pulmonary embolism (2%), pneumothorax, pericarditis (4%), aortic dissection (1%) and esophageal rupture. Other common causes include gastroesophageal reflux disease (30%), muscle or skeletal pain (28%), pneumonia (2%), shingles (0.5%), pleuritis, traumatic and anxiety disorders. Determining the cause of chest pain is based on a persons medical history, a physical exam and other medical tests. About 3% of heart attacks, however, are initially missed.Management of chest pain is based on the underlying cause. Initial treatment often includes the medications aspirin and nitroglycerin. The response to treatment does not usually indicate whether the pain is heart-related. When the cause is unclear, the person may be referred for further evaluation.Chest pain represents about 5% of presenting problems to the emergency room. In the United States, about 8 million people go to the emergency department with chest pain a year. Of these, about 60% are admitted to either the hospital or an observation unit. The cost of emergency visits for chest pain in the United States is more than US$8 billion per year. Chest pain accounts for about 0.5% of visits by children to the emergency department.

Signs and symptoms
Chest pain may present in different ways depending upon the underlying diagnosis. Chest pain may also vary from person to person based upon age, sex, weight, and other differences. Chest pain may present as a stabbing, burning, aching, sharp, or pressure-like sensation in the chest. Chest pain may also radiate, or move, to several other areas of the body. This may include the neck, left or right arms, cervical spine, back, and upper abdomen. Other associated symptoms with chest pain can include nausea, vomiting, dizziness, shortness of breath, anxiety, and sweating. The type, severity, duration, and associated symptoms of chest pain can help guide diagnosis and further treatment.

Differential diagnosis
Causes of chest pain range from non-serious to serious to life-threatening.In adults the most common causes of chest pain include: gastrointestinal (42%), coronary artery disease (31%), musculoskeletal (28%), pericarditis (4%) and pulmonary embolism (2%). Other less common causes include: pneumonia, lung cancer, and aortic aneurysms. Psychogenic causes of chest pain can include panic attacks; however, this is a diagnosis of exclusion.In children, the most common causes for chest pain are musculoskeletal (76-89%), exercise-induced asthma (4-12%), gastrointestinal illness (8%), and psychogenic causes (4%). Chest pain in children can also have congenital causes.

Cardiovascular
Acute coronary syndrome
Stable or unstable angina
Myocardial infarction ("heart attack"): People usually complained of a pressure or squeezing sensation over the chest. Other associated symptoms are: excessive sweating, nausea, vomiting, and weakness. Chest pain is more commonly associated with anterior infarction because of left ventricular impairment; inferior infarction is more commonly associated with nausea, vomiting, and excessive sweating due to irritation of vagus nerve; lateral infarction is associated with left arm pain.
Prinzmetals angina: Chest pain is caused by coronary vasospasm. More common in women younger than 50 years. Person usually complain of chest pain at rest. It may occur early in the morning which awaken person from sleep.
Cocaine use: This condition is suspected when a person with few or no risk of arteriosclerosis presented with non-traumatic chest pain. Ingestion of cocaine can cause vasoconstriction of coronary arteries, thus producing chest pain similar to heart attack. Symptoms can appear within one hour of cocaine use.
Aortic stenosis: This condition happens when the person has underlying congenital bicuspid valve, aortic sclerosis, or history of rheumatic fever. Chest pain usually happens during physical activity. Syncope is a late symptom. Signs and symptoms of heart failure may also present. On auscultation, loud ejection systolic murmur can be best heard at the right second intercostal space and radiates to the carotid artery in the neck. Splitting of second heart sound is heard in severe stenosis.
Hypertrophic cardiomyopathy: It is the hypertrophy of interventricular septum that causes outflow obstruction of left ventricle. Dyspnea and chest pain commonly occurs during daily activities. Sometimes, syncope (fainting) may happen. On physical examination, significant findings include: loud systolic murmur and palpable triple apical impulse due to palpable presystolic fourth heart sound.
Aortic dissection is characterized by severe chest pain that radiates the back. It is usually associated with Marfans syndrome and hypertension. On examination, murmur of aortic insufficiency can be heard with unequal radial pulses.
Pericarditis: This condition can be the result of viral infection such as coxsackie virus and echovirus, tuberculosis, autoimmune disease, uremia, and after myocardial infarction (Dressler syndrome). The chest pain is often pleuritic in nature (associated with respiration) which is aggravated when lying down and relieved on sitting forward, sometimes, accompanied by fever. On auscultation, pericardial friction rub can be heard.
Cardiac tamponade
Arrhythmia: Atrial fibrillation and a number of other arrhythmias can cause chest pain.
Myocarditis
Mitral valve prolapse syndrome: Those affected are usually slim females presented with chest pain which is sharp in quality, localized at the apex, and relieved when lying down. Other symptoms include: shortness of breath, fatigue, and palpitations. On auscultation, midsystolic click followed by late systolic murmur can be heard, louder when person is in standing position.
Aortic aneurysm

Respiratory
Asthma is a common long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. Chest pain usually happens during a strenuous activity or heavy exercise.
Bronchitis
Pulmonary embolism: Common signs and symptoms are shortness of breath, pleuritic chest pain, blood in sputum during cough, and lower limb swelling. Risk factors includes: recent surgery, malignancy, and bedridden state. Source of embolus usually comes from venous thromboembolism.
Pneumonia
Hemothorax
Pneumothorax: Those who are at a higher risk of developing pneumothorax are tall, slim male smokers who have had underlying lung diseases such as emphysema. Those affected can have a sharp chest pain which radiates to the shoulder of the same side. Physical examination revealed absent breath sounds and hyperresonance on the affected side of the chest.
Pleurisy
Tuberculosis
Tracheitis
Lung cancer

Gastrointestinal
Gastroesophageal reflux disease: The pain is aggravated when lying down or after meals. Persons may describe this as a heartburn. Besides, they may also complain of tasting bitter contents from the stomach.
Achalasia, nutcracker esophagus, and other motility disorders of the esophagus
Diffuse esophageal spasm: Unlike cardiac chest pain, esophageal pain is not related to activity. The pain is usually associated with swallowing of hot or cold water.
Esophageal rupture: Those affected usually complain of sudden, severe, and constant pain that starts from the neck to the upper abdomen. The pain is aggravated by swallowing. On examination, neck swelling and crepitations can be felt due to subcutaneous emphysema as free air is entering from esophagus into the subcutaneous tissue.
Esophagitis: There are many causes of esophagitis. Esophagitis caused by Candida albicans is usually found in chemotherapy or HIV patients. Medication such as nonsteroidal anti-inflammatory drug and alendronate can induce esophagitis if not swallowed properly.
Functional dyspepsia
Hiatus hernia
Jackhammer esophagus (hypercontractile peristalsis): Intense long-lasting esophageal muscle spasm.
Acute cholecystitis: Characterized by positive Murphys sign where the person has a cessation of inhalation when the doctor places his finger at the right subcostal region of the abdomen.
Acute pancreatitis: History of excessive alcohol use, cholelithiasis (stones in the gallbladder), and hypertriglyceridemia are risk factors for pancreatitis. It is a constant, boring pain in the upper abdomen.
Perforated peptic ulcer: Sudden onset of severe pain in the upper abdomen which later develops into peritonitis (inflammation of tissues that lines the abdominal organs).
Acute gastritis

Chest wall
Costochondritis or Tietzes syndrome: An inflammation of a costochondral junction. Any movements or palpation of the chest can reproduce the symptoms.
Spinal nerve problem
Fibromyalgia
Chest wall problems
Radiculopathy
Precordial catch syndrome: Another benign and harmless form of a sharp, localized chest pain often mistaken for heart disease.
Breast conditions
Herpes zoster (shingles): It is usually described as a burning sensation over the chest in a unilateral dermatome distribution. However, diagnosis can be difficult because the pain usually appears before the characteristic rash is visible.
Tuberculosis
Osteoarthritis
Bornholm disease
Rib fracture

Psychological
Panic attack: Chest pain is a common symptom of panic attacks, with as high as 78% of persons describing chest pain with their worst panic attacks. Overall chest pain is a symptom of up to 48% of sudden-onset panic attacks, and 10% of gradual-onset panic attacks.
Anxiety
Clinical depression
Somatization disorder
Hypochondria

Others
Hyperventilation syndrome often presents with chest pain and a tingling sensation of the fingertips and around the mouth.
Da costas syndrome
Carbon monoxide poisoning
Sarcoidosis
Lead poisoning
Prolapsed intervertebral disc
Thoracic outlet syndrome
Adverse effect from certain medications

Diagnostic approach
History taking
Knowing a persons risk factors can be extremely useful in ruling in or ruling out serious causes of chest pain. For example, heart attack and thoracic aortic dissection are very rare in healthy individuals under 30 years of age, but significantly more common in individuals with significant risk factors, such as older age, smoking, hypertension, diabetes, history of coronary artery disease or stroke, positive family history (premature atherosclerosis, cholesterol disorders, heart attack at early age), and other risk factors. Chest pain that radiates to one or both shoulders or arms, chest pain that occurs with physical activity, chest pain associated with nausea or vomiting, chest pain accompanied by diaphoresis or sweating, or chest pain described as "pressure," has a higher likelihood of being related to acute coronary syndrome, or inadequate supply of blood to the heart muscle, but even without these symptoms chest pain may be a sign of acute coronary syndrome. Other clues in the history can help lower the suspicion for myocardial infarction. These include chest pain described as "sharp" or "stabbing", chest pain that is positional or pleuritic in nature, and chest pain that can be reproduced with palpation. However, both atypical and typical symptoms of acute coronary syndrome can occur, and in general a history cannot be enough to rule out the diagnosis of acute coronary syndrome. In some cases, chest pain may not even be a symptom of an acute cardiac event. An estimated 33% of persons with myocardial infarction in the United States do not present with chest pain, and carry a significantly higher mortality as a result of delayed treatment.

Physical examination
Careful medical history and physical examination is essential in separating dangerous from trivial causes of disease, and the management of chest pain may be done on specialized units (termed medical assessment units) to concentrate the investigations. Occasionally, invisible medical signs will direct the diagnosis towards particular causes, such as Levines sign in cardiac ischemia. However, in the case of acute coronary syndrome, a third heart sound, diaphoresis, and hypotension are the most strongly associated physical exam findings. However these signs are limited in their prognostic and diagnostic value. Other physical exam findings suggestive of cardiac chest pain may include hypertension, tachycardia, bradycardia, and new heart murmurs. Chest pain that is reproducible during the physical exam with contact of the chest wall is more indicative of non-cardiac chest pain, but still cannot completely rule out acute coronary syndrome. For this reason, in general, additional tests are required to establish the diagnosis.
In the emergency department the typical approach to chest pain involves ruling out the most dangerous causes: heart attack, pulmonary embolism, thoracic aortic dissection, esophageal rupture, tension pneumothorax, and cardiac tamponade.  By elimination or confirmation of the most serious causes, a diagnosis of the origin of the pain may be made. Often, no definite cause will be found and reassurance is then provided.

Risk scores
The Global Registry of Acute Coronary Events score and the Thrombosis in Myocardial Infarction performed at time of admission may help stratify persons into low, intermediate and high risk groups for acute coronary syndrome. However these scores do not provide management guidelines for risk-stratified persons.
The HEART score, stratifies persons into low-risk and high-risk groups, and recommends either discharge or admission based upon the score.
Cumulative score:

0-3: 2.5% risk of adverse cardiac event. Patients can be discharged with follow-up.
4-6: 20.3% risk of adverse cardiac event. Patients should be admitted to the hospital for trending of troponin and provocative testing.
≥7: 72.7% risk of adverse cardiac event, suggesting early invasive measures with these patients and close coordination with inpatient cardiology.If acute coronary syndrome ("heart attack") is suspected, many people are admitted briefly for observation, sequential ECGs, and measurement of cardiac enzymes in the blood over time. On occasion, further tests on follow up may determine the cause.

Medical tests
On the basis of the above, a number of tests may be ordered:
An electrocardiogram (ECG)
Chest radiograph or chest x rays are frequently performed
Echocardiography can be useful in patients with known cardiac disease or aortic dissection
CT scanning is used in the diagnosis of aortic dissection
V/Q scintigraphy or CT pulmonary angiogram (when a pulmonary embolism is suspected)
Blood tests:
Troponin I or T (to indicate myocardial damage)
Complete blood count
Electrolytes and renal function (creatinine)
Liver enzymes
Creatine kinase (and CK-MB fraction in many hospitals)
D-dimer (when suspicion for pulmonary embolism is present but low)
serum lipase to exclude acute pancreatitis

Management
Management of chest pain varies with the underlying cause of the pain and the stage of care.

Prehospital care
Chest pain is a common symptom encountered by emergency medical services. Aspirin increases survival in people with acute coronary syndrome and it is reasonable for EMS dispatchers to recommend it in people with no recent serious bleeding. Supplemental oxygen was used in the past for most people with chest pain but is not needed unless the oxygen saturations are less than 94% or there are signs of respiratory distress. Entonox is frequently used by EMS personnel in the prehospital environment. However, there is little evidence about its effectiveness.

Hospital care
Hospital care of chest pain begins with initial survey of a persons vital signs, airway and breathing, and level of consciousness. This may also include attachment of ECG leads, cardiac monitors, intravenous lines and other medical devices depending on initial evaluation. After evaluation of a persons history, risk factors, physical examination, laboratory testing and imaging, management begins depending on suspected diagnoses. Depending upon the diagnosis, a person may be placed in the intensive care unit, admitted to the hospital, or be treated outpatient. For persons with suspected cardiac chest pain or acute coronary syndrome, or other emergent diagnoses such as pneumothorax, pulmonary embolism, or aortic dissection, admission to the hospital is most often recommended for further treatment.

Outpatient care
For people with non-cardiac chest pain, cognitive behavioral therapy might be helpful on an outpatient basis. A 2015 Cochrane review found that cognitive behavioral therapy might reduce the frequency of chest pain episodes the first three months after treatment. For persons with chest pain due to gastroesophageal reflux disease, a proton-pump inhibitor has been shown to be the most effective treatment. However, treatment with proton pump inhibitors has been shown to be no better than placebo in persons with noncardiac chest pain not caused by gastroesophageal reflux disease. For musculoskeletal causes of chest pain, manipulation therapy or chiropractic therapy, acupuncture,  or a recommendation for increased exercise are often used as treatment </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Motion sickness and explain in detail? [/INST] Motion sickness occurs due to a difference between actual and expected motion. Symptoms commonly include nausea, vomiting, cold sweat, headache, dizziness, tiredness, loss of appetite, and increased salivation. Complications may rarely include dehydration, electrolyte problems, or a lower esophageal tear.The cause of motion sickness is either real or perceived motion. This may include from car travel, air travel, sea travel, space travel, or reality simulation. Risk factors include pregnancy, migraines, and Ménières disease. The diagnosis is based on symptoms.Treatment may include behavioral measures or medications. Behavioral measures include keeping the head still and focusing on the horizon. Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine. Side effects, however, may limit the use of medications. A number of medications used for nausea such as ondansetron are not effective for motion sickness.Nearly all people are affected with sufficient motion and most people will experience motion sickness at least once in their lifetime. Susceptibility, however, is variable, with about one-third of the population being highly susceptible while most other people are affected under extreme conditions. Women are more easily affected than men. Motion sickness has been described since at least the time of Homer (c. eighth century BC).

Signs and symptoms
Symptoms commonly include nausea, vomiting, cold sweat, headache, dizziness, tiredness, loss of appetite, and increased salivation. Occasionally, tiredness can last for hours to days after an episode of motion sickness, known as "sopite syndrome". Rarely severe symptoms such as the inability to walk, ongoing vomiting, or social isolation may occur while rare complications may include dehydration, electrolyte problems, or a lower esophageal tear from severe vomiting.

Cause
Motion sickness can be divided into three categories:
Motion sickness caused by motion that is felt but not seen, as in terrestrial motion sickness;
Motion sickness caused by motion that is seen but not felt, as in space motion sickness;
Motion sickness caused when both systems detect motion but they do not correspond, as in either terrestrial or space motion sickness.

Motion felt but not seen
In these cases, motion is sensed by the vestibular system and hence the motion is felt, but no motion or little motion is detected by the visual system, as in terrestrial motion sickness.

Carsickness
A specific form of terrestrial motion sickness, being carsick is quite common and evidenced by disorientation while reading a map, a book, or a small screen during travel. Carsickness results from the sensory conflict arising in the brain from differing sensory inputs. Motion sickness is caused by a conflict between signals arriving in the brain from the inner ear, which forms the base of the vestibular system, the sensory apparatus that deals with movement and balance, and which detects motion mechanically. If someone is looking at a stationary object within a vehicle, such as a magazine, their eyes will inform their brain that what they are viewing is not moving. Their inner ears, however, will contradict this by sensing the motion of the vehicle.Varying theories exist as to cause. The sensory conflict theory notes that the eyes view motion while riding in the moving vehicle while other body sensors sense stillness, creating conflict between the eyes and inner ear. Another suggests the eyes mostly see the interior of the car which is motionless while the vestibular system of the inner ear senses motion as the vehicle goes around corners or over hills and even small bumps. Therefore, the effect is worse when looking down but may be lessened by looking outside of the vehicle.
In the early 20th century, Austro-Hungarian scientist Róbert Bárány observed the back and forth movement of the eyes of railroad passengers as they looked out the side windows at the scenery whipping by. He called it "railway nystagmus". Also called "optokinetic nystagmus". It causes nausea and vomiting.  His findings were published in the journal Laeger, 83:1516, Nov.17, 1921.

Airsickness
Air sickness is a kind of terrestrial motion sickness induced by certain sensations of air travel. It is a specific form of motion sickness and is considered a normal response in healthy individuals. It is essentially the same as carsickness but occurs in an airplane. An airplane may bank and tilt sharply, and unless passengers are sitting by a window, they are likely to see only the stationary interior of the plane due to the small window sizes and during flights at night. Another factor is that while in flight, the view out of windows may be blocked by clouds, preventing passengers from seeing the moving ground or passing clouds.

Seasickness
Seasickness is a form of terrestrial motion sickness characterized by a feeling of nausea and, in extreme cases, vertigo experienced after spending time on a boat.  It is essentially the same as carsickness, though the motion of a watercraft tends to be more regular. It is typically brought on by the rocking motion of the craft or movement while the craft is immersed in water. As with airsickness, it can be difficult to visually detect motion even if one looks outside the boat since water does not offer fixed points with which to visually judge motion. Poor visibility conditions, such as fog, may worsen seasickness. The greatest contributor to seasickness is the tendency for people being affected by the rolling or surging motions of the craft to seek refuge below decks, where they are unable to relate themselves to the boats surroundings and consequent motion. Some people with carsickness are resistant to seasickness and vice versa. Adjusting to the crafts motion at sea is called "gaining ones sea legs"; it can take a significant portion of the time spent at sea after disembarking to regain a sense of stability "post-sea legs".

Centrifuge motion sickness
Rotating devices such as centrifuges used in astronaut training and amusement park rides such as the Rotor, Mission: Space and the Gravitron can cause motion sickness in many people.  While the interior of the centrifuge does not appear to move, one will experience a sense of motion. In addition, centrifugal force can cause the vestibular system to give one the sense that downward is in the direction away from the center of the centrifuge rather than the true downward direction.

Dizziness due to spinning
When one spins and stops suddenly, fluid in the inner ear continues to rotate causing a sense of continued spinning while ones visual system no longer detects motion.

Virtual reality
Usually, VR programs would detect the motion of the users head and adjust the rotation of vision to avoid dizziness. However, some cases such as system lagging or software crashing could cause lags in the screen updates. In such cases, even some small head motions could trigger the motion sickness by the defense mechanism mentioned below: the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still.

Motion seen but not felt
In these cases, motion is detected by the visual system and hence the motion is seen, but no motion or little motion is sensed by the vestibular system. Motion sickness arising from such situations has been referred to as "visually induced motion sickness" (VIMS).

Space motion sickness
Zero gravity interferes with the vestibular systems gravity-dependent operations, so that the two systems, vestibular and visual, no longer provide a unified and coherent sensory representation. This causes unpleasant disorientation sensations often quite distinct from terrestrial motion sickness, but with similar symptoms. The symptoms may be more intense because a condition caused by prolonged weightlessness is usually quite unfamiliar.Space motion sickness was effectively unknown during the earliest spaceflights because the very cramped conditions of the spacecraft allowed for only minimal bodily motion, especially head motion. Space motion sickness seems to be aggravated by being able to freely move around, and so is more common in larger spacecraft. Around 60% of Space Shuttle astronauts experienced it on their first flight; the first case of space motion sickness is now thought to be the Soviet cosmonaut Gherman Titov, in August 1961 onboard Vostok 2, who reported dizziness, nausea, and vomiting. The first severe cases were in early Apollo flights; Frank Borman on Apollo 8 and Rusty Schweickart on Apollo 9. Both experienced identifiable and quite unpleasant symptoms—in the latter case causing the mission plan to be modified.

Screen images
This type of terrestrial motion sickness is particularly prevalent when susceptible people are watching films presented on very large screens such as IMAX, but may also occur in regular format theaters or even when watching TV or playing games.  For the sake of novelty, IMAX and other panoramic type theaters often show dramatic motions such as flying over a landscape or riding a roller coaster.  This type of motion sickness can be prevented by closing ones eyes during such scenes.In regular-format theaters, an example of a movie that caused motion sickness in many people is The Blair Witch Project.  Theaters warned patrons of its possible nauseating effects, cautioning pregnant women in particular.  Blair Witch was filmed with a handheld camcorder, which was subjected to considerably more motion than the average movie camera, and lacks the stabilization mechanisms of steadicams.Home movies, often filmed with a cell phone camera, also tend to cause motion sickness in those who view them.  The person holding the cell phone or other camera usually is unaware of this as the recording is being made since the sense of motion seems to match the motion seen through the cameras viewfinder.  Those who view the film afterward only see the movement, which may be considerable, without any sense of motion.  Using the zoom function seems to contribute to motion sickness as well since zooming is not a normal function of the eye.  The use of a tripod or a camera or cell phone with image stabilization while filming can reduce this effect.

Virtual reality
Motion sickness due to virtual reality is very similar to simulation sickness and motion sickness due to films.  In virtual reality the effect is made more acute as all external reference points are blocked from vision, the simulated images are three-dimensional and in some cases stereo sound that may also give a sense of motion. The NADS-1, a simulator located at the National Advanced Driving Simulator, is capable of accurately stimulating the vestibular system with a 360-degree horizontal field of view and 13 degrees of freedom motion base. Studies have shown that exposure to rotational motions in a virtual environment can cause significant increases in nausea and other symptoms of motion sickness.In a study conducted by the U.S. Army Research Institute for the Behavioral and Social Sciences in a report published May 1995 titled "Technical Report 1027 – Simulator Sickness in Virtual Environments", out of 742 pilot exposures from 11 military flight simulators, "approximately half of the pilots (334) reported post-effects of some kind: 250 (34%) reported that symptoms dissipated in less than one hour, 44 (6%) reported that symptoms lasted longer than four hours, and 28 (4%) reported that symptoms lasted longer than six hours. There were also four (1%) reported cases of spontaneously occurring flashbacks."

Motion that is seen and felt
When moving within a rotating reference frame such as in a centrifuge or environment where gravity is simulated with centrifugal force, the coriolis effect causes a sense of motion in the vestibular system that does not match the motion that is seen.

Pathophysiology
There are various hypotheses that attempt to explain the cause of the condition.

Sensory conflict theory
Contemporary sensory conflict theory, referring to "a discontinuity between either visual, proprioceptive, and somatosensory input, or semicircular canal and otolith input", is probably the most thoroughly studied. According to this theory, when the brain presents the mind with two incongruous states of motion; the result is often nausea and other symptoms of disorientation known as motion sickness. Such conditions happen when the vestibular system and the visual system do not present a synchronized and unified representation of ones body and surroundings.According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness. The former occurs when one perceives visually that ones surroundings are relatively immobile while the vestibular system reports that ones body is in motion relative to its surroundings. The latter can occur when the visual system perceives that ones surroundings are in motion while the vestibular system reports relative bodily immobility (as in zero gravity.)

Neural mismatch
A variation of the sensory conflict theory is known as neural mismatch, implying a mismatch occurring between ongoing sensory experience and long-term memory rather than between components of the vestibular and visual systems. This theory emphasizes "the limbic system in the integration of sensory information and long-term memory, in the expression of the symptoms of motion sickness, and the impact of anti-motion-sickness drugs and stress hormones on limbic system function. The limbic system may be the neural mismatch center of the brain."

Defense against poisoning
It has also been proposed that motion sickness could function as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in the cabin of a ship with no portholes), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treismans indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the bodys poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

Nystagmus hypothesis
Yet another theory, known as the nystagmus hypothesis, has been proposed based on stimulation of the vagus nerve resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eyes six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherringtons Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherringtons Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, tenth nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherringtons Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.A recent theory  argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in free fall) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic).

Diagnosis
The diagnosis is based on symptoms. Other conditions that may present similarly include vestibular disorders such as benign paroxysmal positional vertigo and vestibular migraine and stroke.

Treatment
Treatment may include behavioral measures or medications.

Behavioral measures
Behavioral measures to decrease motion sickness include holding the head still and lying on the back. Focusing on the horizon may also be useful. Listening to music, mindful breathing, being the driver, and not reading while moving are other techniques.Habituation is the most effective technique but requires significant time. It is often used by the military for pilots. These techniques must be carried out at least every week to retain effectiveness.A head-worn, computer device with a transparent display can be used to mitigate the effects of motion sickness (and spatial disorientation) if visual indicators of the wearers head position are shown. Such a device functions by providing the wearer with digital reference lines in their field of vision that indicate the horizons position relative to the users head. This is accomplished by combining readings from accelerometers and gyroscopes mounted in the device. This technology has been implemented in both standalone devices and Google Glass. One promising looking treatment is to wear LCD shutter glasses that create a stroboscopic vision of 4 Hz with a dwell of 10 milliseconds.

Medication
Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine. Benefits are greater if used before the onset of symptoms or shortly after symptoms begin. Side effects, however, may limit the use of medications. A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness.Scopolamine is the most effective medication. Evidence is best for when it is used preventatively. It is available as a skin patch. Side effects may include blurry vision.Other effective first generation antihistamines include doxylamine, diphenhydramine, promethazine, meclizine, cyclizine, and cinnarizine. In pregnancy meclizine, dimenhydrinate and doxylamine are generally felt to be safe. Side effects include sleepiness. Second generation antihistamines have not been found to be useful.Dextroamphetamine may be used together with an antihistamine or an antimuscarinic. Concerns include their addictive potential.Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications. Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail".

Alternative medicine
Alternative treatments include acupuncture and ginger although their effectiveness against motion sickness is variable. Providing smells does not appear to have a significant effect on the rate of motion sickness.

Epidemiology
Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions. Around 80% of the general population is susceptible to cases of medium to high motion sickness </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Myelitis and explain in detail? [/INST] Myelitis is inflammation of the spinal cord which can disrupt the normal responses from the brain to the rest of the body, and from the rest of the body to the brain. Inflammation in the spinal cord, can cause the myelin and axon to be damaged resulting in symptoms such as paralysis and sensory loss. Myelitis is classified to several categories depending on the area or the cause of the lesion; however, any inflammatory attack on the spinal cord is often referred to as transverse myelitis.

Types of myelitis
Myelitis lesions usually occur in a narrow region but can be spread and affect many areas.

Acute flaccid myelitis: a polio-like syndrome that causes muscle weakness and paralysis.
Poliomyelitis: disease caused by viral infection in the gray matter with symptoms of muscle paralysis or weakness
Transverse myelitis: caused by axonal demyelination encompassing both sides of the spinal cord
Leukomyelitis: lesions in the white matter
Meningococcal myelitis (or meningomyelitis): lesions occurring in the region of meninges and the spinal cordOsteomyelitis of the vertebral bone surrounding the spinal cord (that is, vertebral osteomyelitis) is a separate condition, although some infections (for example, Staphylococcus aureus infection) can occasionally cause both at once. The similarity of the words reflects that the combining form myel(o)- has multiple (homonymous) senses referring to bone marrow or the spinal cord.

Symptoms
Depending on the cause of the disease, such clinical conditions manifest different speed in progression of symptoms in a matter of hours to days. Most myelitis manifests fast progression in muscle weakness or paralysis starting with the legs and then arms with varying degrees of severity. Sometimes the dysfunction of arms or legs cause instability of posture and difficulty in walking or any movement. Also symptoms generally include paresthesia which is a sensation of tickling, tingling, burning, pricking, or numbness of a persons skin with no apparent long-term physical effect. Adult patients often report pain in the back, extremities, or abdomen. Patients also present increased urinary urgency, bowel or bladder dysfunctions such as bladder incontinence, difficulty or inability to void, and incomplete evacuation of bowel or constipation. Others also report fever, respiratory problems and intractable vomiting.

Diseases associated with myelitis
Conditions associated with myelitis include:

Acute disseminated encephalomyelitis: autoimmune demyelination of the brain causing severe neurological signs and symptoms
Multiple sclerosis: demyelination of the brain and spinal cord
Neuromyelitis optica or Devics disease: immune attack on optic nerve and spinal cord
Sjögrens syndrome: destruction of the exocrine system of the body
Systemic lupus erythematosus: a systemic autoimmune disease featuring a wide variety of neurological signs and symptoms
Sarcoidosis: chronic inflammatory cells form as nodules in multiple organs
Atopy: an immune disorder of children manifesting as eczema or other allergic conditions. It can include atopic myelitis, which causes weakness.
Immune-mediated myelopathies, heterogeneous group of inflammatory spinal cord disorders including autoimmune disorders with known antibodies

Cause
Myelitis occurs due to various reasons such as infections. Direct infection by viruses, bacteria, mold, or parasites such as human immunodeficiency virus (HIV), human T-lymphotropic virus types I and II (HTLV-I/II), syphilis, lyme disease, and tuberculosis can cause myelitis but it can also be caused due to non-infectious or inflammatory pathway. Myelitis often follows after the infections or after vaccination. These phenomena can be explained by a theory of autoimmune attack which states that the autoimmune bodies attack its spinal cord in response to immune reaction.

Mechanism of myelitis
The theory of autoimmune attack claims that a person with neuroimmunologic disorders have genetic predisposition to auto-immune disorder, and the environmental factors would trigger the disease. The specific genetics in myelitis is not completely understood. It is believed that the immune system response could be to viral, bacterial, fungal, or parasitic infection; however, it is not known why the immune system attacks itself. Especially, for the immune system to cause inflammatory response anywhere in the central nervous system, the cells from the immune system must pass through the blood brain barrier. In the case of myelitis, not only is the immune system dysfunctional, but the dysfunction also crosses this protective blood brain barrier to affect the spinal cord.

Infectious myelitis
Viral myelitisMost viral myelitis is acute, but the retroviruses (such as HIV and HTLV) can cause chronic myelitis. Poliomyelitis, or gray matter myelitis, is usually caused by infection of anterior horn of the spinal cord by the enteroviruses (polioviruses, enteroviruses (EV) 70 and 71, echoviruses, coxsackieviruses A and B) and the flaviviruses (West Nile, Japanese encephalitis, tick-borne encephalitis). On the other hand, transverse myelitis or leukomyelitis, or white matter myelitis, are often caused by the herpesviruses and influenza virus. It can be due to direct viral invasion or via immune mediated mechanisms.

Bacterial myelitisBacterial myelitis includes Mycoplasma pneumoniae, which is a common agent for respiratory tract. Studies have shown respiratory tract infections within 4–39 days prior to the onset of transverse myelitis. Or, tuberculosis, syphilis, and brucellosis are also known to cause myelitis in immune-compromised individuals. Myelitis is a rare manifestation of bacterial infection.

Fungal myelitisFungi have been reported to cause spinal cord disease either by forming abscesses inside the bone or by granuloma. In general, there are two groups of fungi that may infect the CNS and cause myelitis - primary and secondary pathogens. Primary pathogens include the following: Cryptococcus neoformans, Coccidioides immitis, Blastomyces dermatitides, and Hystoplasma capsulatum. Secondary pathogens are opportunistic agents that primarily infect immunocompromised hosts such as Candida species, Aspergillus species, and zygomycetes.

Parasitic myelitisParasitic species infect human hosts through larvae that penetrate the skin. Then they enter the lymphatic and circulatory system, and migrate to liver and lung. Some reach the spinal cord. Parasitic infections have been reported with Schistosoma species, Toxocara canis, Echinococcus species, Taenia solium, Trichinella spiralis, and Plasmodium species.

Autoimmune myelitis
In 2016, it was identified in Mayo clinic an autoimmune form of myelitis due to the presence of anti-GFAP autoantibodies. Immunoglobulins directed against the α-isoform of glial fibrillary acidic protein (GFAP-IgG) predicted a special meningoencephalomyelitis termed autoimmune GFAP Astrocytopathy that later was found also to be able to appear as a myelitis.

Diagnosis
Myelitis has an extensive differential diagnosis. The type of onset (acute versus subacute/chronic) along with associated symptoms such as the presence of pain, constitutional symptoms that encompass fever, malaise, weight loss or a cutaneous rash may help identify the cause of myelitis. In order to establish a diagnosis of myelitis, one has to localize the spinal cord level, and exclude cerebral and neuromuscular diseases. Also a detailed medical history, a careful neurologic examination, and imaging studies using magnetic resonance imaging (MRI) are needed. In respect to the cause of the process, further work-up would help identify the cause and guide treatment. Full spine MRI is warranted, especially with acute onset myelitis, to evaluate for structural lesions that may require surgical intervention, or disseminated disease. Adding gadolinium further increases diagnostic sensitivity. A brain MRI may be needed to identify the extent of central nervous system (CNS) involvement. Lumbar puncture is important for the diagnosis of acute myelitis when a tumoral process, inflammatory or infectious cause are suspected, or the MRI is normal or non-specific. Complementary blood tests are also of value in establishing a firm diagnosis. Rarely, a biopsy of a mass lesion may become necessary when the cause is uncertain. However, in 15–30% of people with subacute or chronic myelitis, a clear cause is never uncovered.

Treatment
Since each case is different, the following are possible treatments that patients might receive in the management of myelitis.

Intravenous steroidsHigh-dose intravenous methyl-prednisolone for 3–5 days is considered as a standard of care for patients suspected to have acute myelitis, unless there are compelling reasons otherwise. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of five days of steroids.
Plasma exchange (PLEX)Patients with moderate to aggressive forms of disease who do not show much improvement after being treated with intravenous and oral steroids will be treated with PLEX. Retrospective studies of patients with TM treated with IV steroids followed by PLEX showed a positive outcome. It also has been shown to be effective with other autoimmune or inflammatory central nervous system disorders. Particular benefit has been shown with patients who are in the acute or subacute stage of the myelitis showing active inflammation on MRI. However, because of the risks implied by the lumbar puncture procedure, this intervention is determined by the treating physician on a case-by-case basis.
Immunosuppressants/Immunomodulatory agentsMyelitis with no definite cause seldom recurs, but for others, myelitis may be a manifestation of other diseases that are mentioned above. In these cases, ongoing treatment with medications that modulate or suppress the immune system may be necessary. Sometimes there is no specific treatment. Either way, aggressive rehabilitation and long-term symptom management are an integral part of the healthcare plan.

Prospective research direction
Central nervous system nerve regeneration would be able to repair or regenerate the damage caused to the spinal cord. It would restore functions lost due to the disease.
Engineering endogenous repairCurrently, there exists a hydrogel based scaffold which acts as a channel to deliver nerve growth-enhancing substrates while providing structural support. These factors would promote nerve repairs to the target area. Hydrogels macroporous properties would enable attachment of cells and enhance ion and nutrient exchange. In addition, hydrogels biodegradability or bioresolvability would prevent the need for surgical removal of the hydrogel after drug delivery </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chédiak–Higashi syndrome and explain in detail? [/INST] Chédiak–Higashi syndrome (CHS) is a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein, which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism, and peripheral neuropathy.
In Chédiak–Higashi syndrome, the lysosomal trafficking regulator (LYST) gene is mutated, leading to disruption of protein synthesis as well as the storage and secretory function of lysosomal granules in white blood cells. This results in defective white blood cell function with enlarged vesicles. This syndrome also leads to neutropenia and phagocyte bactericidal dysfunction due to impaired chemotaxis. Deficiency in serotonin and adenosine-phosphate-containing granules in platelets causes impaired platelet aggregation, leading to prolonged bleeding time. Thus, patients are susceptible to infections and often present with oculo-cutaneous albinism and coagulation defects. Patients often present with early-onset aggressive periodontitis associated with advanced alveolar bone loss and tooth mobility due to neutropenia and defective neutrophil function. Recurrent oral ulcerations are also one of the common oral manifestations in patients with this disease. Dental practitioners who notice child patients who present with recurrent unexplained gingivitis and periodontitis along with hypopigmentation of hair, skin and eyes should consider making a referral to medical practitioners to investigate for the possible diagnosis of Chédiak–Higashi syndrome.

Signs and symptoms
People with CHS have light skin and silvery hair (albinism) and frequently complain of solar sensitivity and photophobia. Other signs and symptoms vary considerably, but frequent infections and neuropathy are common. The infections involve mucous membranes, skin, and the respiratory tract. Affected children are susceptible to infection by Gram-positive and gram-negative bacteria and fungi, with Staphylococcus aureus being the most common infectious cause. Infections in CHS patients tend to be very serious and even life-threatening. Neuropathy often begins in the teenage years and becomes the most prominent problem. Few patients with this condition live to adulthood.Most children with Chédiak–Higashi syndrome ultimately reach a stage known as the "accelerated phase", or the "lymphoma-like syndrome", in which defective white blood cells divide uncontrollably and invade many of the bodys organs. The accelerated phase is associated with fever, episodes of abnormal bleeding, overwhelming infections, and organ failure. These medical problems are usually life-threatening in childhood.

Causes
Mutations in the CHS1 gene (also called LYST) located on the chromosome 1q42-q43 have been found to be connected with Chédiak–Higashi syndrome. This gene provides instructions for making a protein known as the lysosomal trafficking regulator. Researchers believe that this protein plays a role in the transport (trafficking) of materials into lysosomes. Lysosomes act as recycling centers within cells. They use digestive enzymes to break down toxic substances, digest bacteria that invade the cell and recycle worn-out cell components. Although the lysosomal trafficking regulator protein is involved in the normal function of lysosomes, its exact role is unknown.In melanocytic cells, LYST gene expression may be regulated by MITF. Mutations in MITF are known to cause Waardenburg syndrome type 2 and Tietz syndrome, which result in depigmentation and deafness.

Pathophysiology
CHS is a disease causing impaired bacteriolysis due to failure of phagolysosome formation. As a result of disordered intracellular trafficking there is impaired lysosome degranulation with phagosomes, so phagocytosed bacteria are not destroyed by the lysosomes enzymes.In addition, secretion of lytic secretory granule by cytotoxic T cells is affected.The disease is characterised by large lysosome vesicles in phagocytes (neutrophils), which thus have poor bactericidal function, leading to susceptibility to infections, abnormalities in nuclear structure of leukocytes, anemia, and hepatomegaly. Döhle bodies (remnants of endoplasmic reticulum) in the neutrophil are also seen.

Diagnosis
The diagnosis is confirmed by bone marrow smears that show "giant inclusion bodies" in the cells that develop into white blood cells (leukocyte precursor cells). CHS can be diagnosed prenatally by examining a sample of hair from a fetal scalp biopsy or testing leukocytes from a fetal blood sample.Under light microscopy the hairs present evenly distributed, regular melanin granules, larger than those found in normal hairs </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sleep state misperception and explain in detail? [/INST] Sleep state misperception (SSM) is a term in the International Classification of Sleep Disorders (ICSD) most commonly used for people who mistakenly perceive their sleep as wakefulness, though it has been proposed that it be applied to those who severely overestimate their sleep time as well ("positive" sleep state misperception). While most sleepers with this condition will report not having slept in the previous night at all or having slept very little, clinical recordings generally show normal sleep patterns. Though the sleep patterns found in those with SSM have long been considered indistinguishable from those without, some preliminary research suggest there may be subtle differences (see Symptoms and diagnosis: Spectral analysis).Patients are otherwise generally in good  health, and any illnesses—such as depression—appear to be more associated with fear of negative consequences of insomnia ("insomnia phobia") than from any actual loss of sleep.Sleep state misperception was adopted by the ICSD to replace two previous diagnostic terminologies: "subjective insomnia complaint without objective findings" and "subjective sleepiness complaint without objective findings."The validity and reliability of sleep state misperception as a pertinent diagnosis has been questioned, with studies finding poor empirical support.

Classification
Sleep state misperception is classified as an intrinsic dyssomnia. While SSM is regarded a sub-type of insomnia, it is also established as a separate sleep-condition, with distinct pathophysiology. Nonetheless, the value of distinguishing this type of insomnia from other types is debatable due to the relatively low frequency of SSM being reported.Sleep state misperception can also be further broken down into several types, by patients who:

report short sleep (subjective insomnia complaint without objective findings)or no sleep at all (subjective total insomnia)
report excessive daytime sleepiness (subjective sleepiness complaint without objective findings)
report sleeping too much (subjective hypersomnia without objective findings)

Validity
The validity and reliability of the sleep state misperception as a pertinent medical entity was questioned. A study found poor empirical support for this diagnostic item.

Symptoms and diagnosis
This sleep disorder frequently applies when patients report not feeling tired despite their subjective perception of not having slept. Generally, they may describe experiencing several years of no sleep, short sleep, or non-restorative sleep. Otherwise, patients appear healthy, both psychiatrically and medically. (That this condition is often asymptomatic could explain why it is relatively unreported.)
However, upon clinical observation, it is found that patients may severely overestimate the time they took to fall asleep—often reporting having slept half the amount of time indicated by polysomnogram or electroencephalography (EEG), which may record normal sleep. Observing such discrepancy between subjective and objective reports, clinicians may conclude that the perception of poor sleep is primarily illusionary.
Alternatively, some people may report excessive daytime sleepiness or chronic disabling sleepiness, while no sleep disorder has been found to exist. Methods of diagnosing sleepiness objectively, such as the Multiple Sleep Latency Test, do not confirm the symptom—objective sleepiness is not observed despite the complaint.Finally, on the opposite end of the spectrum, other patients may report feeling that they have slept much longer than is observed. It has been proposed that this experience be subclassified under sleep state misperception as "positive sleep state misperception", "reverse sleep state misperception", and "negative sleep state misperception".

Diagnostic criteria
The patient has a complaint of insomnia while sleep quality and duration are normal. Polysomnographic monitoring demonstrates normal sleep latency, a normal number of arousals and awakenings, and normal sleep duration with or without a multiple sleep latency test that demonstrates a mean sleep latency of greater than 10 minutes. No medical or mental disorder produces the complaint. Other sleep disorders producing insomnia are not present to a degree that would explain the patient’s complaint.

Detection and difficulties
Detecting sleep state misperception by objective means has been elusive.A 2011 study published in the journal Psychosomatic Medicine has shown that sleep misperception (i.e., underestimation of sleep duration) is prevalent among chronic insomniacs who sleep objectively more than 6 hours in the sleep lab. The psychological profile of these chronic insomniacs with objective normal sleep duration is characterized by depressive, anxious-ruminative traits and poor coping resources. Thus, it appears that not all chronic insomniacs underestimate their sleep duration, and that sleep misperception is a clinical characteristic of chronic insomniacs with objective normal sleep duration. Furthermore, rumination and poor coping resources may play a significant role in sleep misperception.

Spectral analysis
According to a May 2014 article published in New Scientist, spectral analysis may help clinicians find objective evidence for sleep state misperception:

[...] it uncovered [...] subtle differences in the EEGs of sleeping insomniacs: alpha waves – signatures of wakefulness that are supposed to show up only in early sleep – were intruding into deep sleep. [...] [psychologist and sleep researcher Michael] Perlis. But Andrew Krystal of Duke University in Durham, North Carolina, used spectral analysis to quantify just how much they were intruding.  Krystals non-sleepers not only had a greater proportion of these alpha disturbances, but the alpha waves were bigger and the delta waves were correspondingly smaller.  That wasnt all. When Perlis and other researchers applied spectral analysis algorithms to the EEGs of their sleeping insomniacs, they found different patterns, fast waves known as beta and gamma (Sleep, vol 24, p 110). Normally, these are indicators of consciousness, alertness and even anxiety [...] Like alpha waves, Perlis calls these beta and gamma waves "intrusions" into normal sleep: "Its as if somebody is playing with the switch – boop, boop – flipping at a mad rate between wake and sleep".

Distinction from insomnia
What is considered objective insomnia, unlike SSM, can easily be confirmed empirically through clinical testing, such as by polysomnogram. Those who experience SSM may believe that they have not slept for extended periods of time, when they in fact do sleep but without perceiving it </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Blizzard and explain in detail? [/INST] A blizzard is a severe snowstorm characterized by strong sustained winds and low visibility, lasting for a prolonged period of time—typically at least three or four hours. A ground blizzard is a weather condition where snow is not falling but loose snow on the ground is lifted and blown by strong winds. Blizzards can have an immense size and usually stretch to hundreds or thousands of kilometres.

Definition and etymology
In the United States, the National Weather Service defines a blizzard as a severe snow storm characterized by strong winds causing blowing snow that results in low visibilities. The difference between a blizzard and a snowstorm is the strength of the wind, not the amount of snow. To be a blizzard, a snow storm must have sustained winds or frequent gusts that are greater than or equal to 56 km/h (35 mph) with blowing or drifting snow which reduces visibility to 400 m or 0.25 mi or less and must last for a prolonged period of time—typically three hours or more.
Environment Canada defines a blizzard as a storm with wind speeds exceeding 40 km/h (25 mph) accompanied by visibility of 400 metres (0.25 mi) or less, resulting from snowfall, blowing snow, or a combination of the two. These conditions must persist for a period of at least four hours for the storm to be classified as a blizzard, except north of the arctic tree line, where that threshold is raised to six hours.
The Australia Bureau of Meteorology describes a blizzard as, "Violent and very cold wind which is laden with snow, some part, at least, of which has been raised from snow covered ground."

While severe cold and large amounts of drifting snow may accompany blizzards, they are not required. Blizzards can bring whiteout conditions, and can paralyze regions for days at a time, particularly where snowfall is unusual or rare.
A severe blizzard has winds over 72 km/h (45 mph), near zero visibility, and temperatures of −12 °C (10 °F) or lower. In Antarctica, blizzards are associated with winds spilling over the edge of the ice plateau at an average velocity of 160 km/h (99 mph).Ground blizzard refers to a weather condition where loose snow or ice on the ground is lifted and blown by strong winds. The primary difference between a ground blizzard as opposed to a regular blizzard is that in a ground blizzard no precipitation is produced at the time, but rather all the precipitation is already present in the form of snow or ice at the surface.
The Oxford English Dictionary concludes the term blizzard is likely onomatopoeic, derived from the same sense as blow, blast, blister, and bluster; the first recorded use of it for weather dates to 1829, when it was defined as a "violent blow". It achieved its modern definition by 1859, when it was in use in the western United States. The term became common in the press during the harsh winter of 1880–81.

United States storm systems
In the United States, storm systems powerful enough to cause blizzards usually form when the jet stream dips far to the south, allowing cold, dry polar air from the north to clash with warm, humid air moving up from the south.When cold, moist air from the Pacific Ocean moves eastward to the Rocky Mountains and the Great Plains, and warmer, moist air moves north from the Gulf of Mexico, all that is needed is a movement of cold polar air moving south to form potential blizzard conditions that may extend from the Texas Panhandle to the Great Lakes and Midwest. A blizzard also may be formed when a cold front and warm front mix together and a blizzard forms at the border line.
Another storm system occurs when a cold core low over the Hudson Bay area in Canada is displaced southward over southeastern Canada, the Great Lakes, and New England. When the rapidly moving cold front collides with warmer air coming north from the Gulf of Mexico, strong surface winds, significant cold air advection, and extensive wintry precipitation occur.

Low pressure systems moving out of the Rocky Mountains onto the Great Plains, a broad expanse of flat land, much of it covered in prairie, steppe and grassland, can cause thunderstorms and rain to the south and heavy snows and strong winds to the north. With few trees or other obstructions to reduce wind and blowing, this part of the country is particularly vulnerable to blizzards with very low temperatures and whiteout conditions. In a true whiteout there is no visible horizon. People can become lost in their own front yards, when the door is only 3 m (10 ft) away, and they would have to feel their way back. Motorists have to stop their cars where they are, as the road is impossible to see.

Noreaster blizzards
A noreaster is a macro-scale storm that occurs off the New England and Atlantic Canada coastlines. It gets its name from the direction the wind is coming from. The usage of the term in North America comes from the wind associated with many different types of storms some of which can form in the North Atlantic Ocean and some of which form as far south as the Gulf of Mexico. The term is most often used in the coastal areas of New England and Atlantic Canada. This type of storm has characteristics similar to a hurricane. More specifically it describes a low-pressure area whose center of rotation is just off the coast and whose leading winds in the left-forward quadrant rotate onto land from the northeast. High storm waves may sink ships at sea and cause coastal flooding and beach erosion. Notable noreasters include The Great Blizzard of 1888, one of the worst blizzards in U.S. history. It dropped 100–130 cm (40–50 in) of snow and had sustained winds of more than 45 miles per hour (72 km/h) that produced snowdrifts in excess of 50 feet (15 m). Railroads were shut down and people were confined to their houses for up to a week. It killed 400 people, mostly in New York.

Historic events
1972 Iran blizzard
The 1972 Iran blizzard, which caused 4,000 reported deaths, was the deadliest blizzard in recorded history. Dropping as much as 26 feet (7.9 m) of snow, it completely covered 200 villages. After a snowfall lasting nearly a week, an area the size of Wisconsin was entirely buried in snow.

2008 Afghanistan blizzard
The 2008 Afghanistan blizzard, was a fierce blizzard that struck Afghanistan on the 10th of January 2008. Temperatures fell to a low of −30 °C (−22 °F), with up to 180 centimetres (71 in) of snow in the more mountainous regions, killing at least 926 people. It was the third deadliest blizzard in history. The weather also claimed more than 100,000 sheep and goats, and nearly 315,000 cattle died.

The Snow Winter of 1880–1881
The winter of 1880–1881 is widely considered the most severe winter ever known in parts of the United States. Many children—and their parents—learned of "The Snow Winter" through the childrens book The Long Winter by Laura Ingalls Wilder, in which the author tells of her familys efforts to survive. The snow arrived in October 1880 and blizzard followed blizzard throughout the winter and into March 1881, leaving many areas snowbound throughout the entire winter. Accurate details in Wilders novel include the blizzards frequency and the deep cold, the Chicago and North Western Railway stopping trains until the spring thaw because the snow made the tracks impassable, the near-starvation of the townspeople, and the courage of her future husband Almanzo and another man, who ventured out on the open prairie in search of a cache of wheat that no one was even sure existed.
The October blizzard brought snowfalls so deep that two-story homes had snow up to the second floor windows. No one was prepared for the deep snow so early in the season and farmers all over the region were caught before their crops had even been harvested, their grain milled, or with their fuel supplies for the winter in place. By January the train service was almost entirely suspended from the region. Railroads hired scores of men to dig out the tracks but it was a wasted effort: As soon as they had finished shoveling a stretch of line, a new storm arrived, filling up the line and leaving their work useless.

There were no winter thaws and on February 2, 1881, a second massive blizzard struck that lasted for nine days. In the towns the streets were filled with solid drifts to the tops of the buildings and tunneling was needed to secure passage about town. Homes and barns were completely covered, compelling farmers to tunnel to reach and feed their stock.
When the snow finally melted in late spring of 1881, huge sections of the plains were flooded. Massive ice jams clogged the Missouri River and when they broke the downstream areas were ravaged. Most of the town of Yankton, in what is now South Dakota, was washed away when the river overflowed its banks.

The Storm of the Century
The Storm of the Century, also known as the Great Blizzard of 1993, was a large cyclonic storm that formed over the Gulf of Mexico on March 12, 1993, and dissipated in the North Atlantic Ocean on March 15. It is unique for its intensity, massive size and wide-reaching effect. At its height, the storm stretched from Canada towards Central America, but its main impact was on the United States and Cuba. The cyclone moved through the Gulf of Mexico, and then through the Eastern United States before moving into Canada. Areas as far south as northern Alabama and Georgia received a dusting of snow and areas such as Birmingham, Alabama, received up to 12 in (30 cm)  with hurricane-force wind gusts and record low barometric pressures. Between Louisiana and Cuba, hurricane-force winds produced high storm surges across northwestern Florida, which along with scattered tornadoes killed dozens of people. In the United States, the storm was responsible for the loss of electric power to over 10 million customers. It is purported to have been directly experienced by nearly 40 percent of the countrys population at that time. A total of 310 people, including 10 from Cuba, perished during this storm. The storm cost $6 to $10 billion in damages.

List of blizzards
North America
1700 to 1799
The Great Snow 1717 series of four snowstorms between February 27 and March 7, 1717. There were reports of about five feet of snow already on the ground when the first of the storms hit. By the end, there were about ten feet of snow and some drifts reaching 25 feet (7.6 m), burying houses entirely. In the colonial era, this storm made travel impossible until the snow simply melted.
Blizzard of 1765. March 24, 1765. Affected area from Philadelphia to Massachusetts. High winds and over 2 feet (61 cm) of snowfall recorded in some areas.
Blizzard of 1772. "The Washington and Jefferson Snowstorm of 1772". January 26–29, 1772. One of largest D.C. and Virginia area snowstorms ever recorded. Snow accumulations of 3 feet (91 cm) recorded.
The "Hessian Storm of 1778". December 26, 1778. Severe blizzard with high winds, heavy snows and bitter cold extending from Pennsylvania to New England. Snow drifts reported to be 15 feet (4.6 m) high in Rhode Island. Storm named for stranded Hessian troops in deep snows stationed in Rhode Island during the Revolutionary War.
The Great Snow of 1786. December 4–10, 1786. Blizzard conditions and a succession of three harsh snowstorms produced snow depths of 2 feet (61 cm) to 4 feet (120 cm) from Pennsylvania to New England. Reportedly of similar magnitude of 1717 snowstorms.
The Long Storm of 1798. November 19–21, 1798. Heavy snowstorm produced snow from Maryland to Maine.

1800 to 1850
Blizzard of 1805. January 26–28, 1805. Cyclone brought heavy snowstorm to New York City and New England. Snow fell continuously for two days where over 2 feet (61 cm) of snow accumulated.
New York City Blizzard of 1811. December 23–24, 1811. Severe blizzard conditions reported on Long Island, in New York City, and southern New England. Strong winds and tides caused damage to shipping in harbor.
Luminous Blizzard of 1817. January 17, 1817. In Massachusetts and Vermont, a severe snowstorm was accompanied by frequent lightning and heavy thunder. St. Elmos fire reportedly lit up trees, fence posts, house roofs, and even people. John Farrar professor at Harvard, recorded the event in his memoir in 1821.
Great Snowstorm of 1821. January 5–7, 1821. Extensive snowstorm and blizzard spread from Virginia to New England.
Winter of Deep Snow in 1830. December 29, 1830. Blizzard storm dumped 36 inches (91 cm) in Kansas City and 30 inches (76 cm) in Illinois. Areas experienced repeated storms thru mid-February 1831.
"The Great Snowstorm of 1831" January 14–16, 1831. Produced snowfall over widest geographic area that was only rivaled, or exceeded by, the 1993 Blizzard. Blizzard raged from Georgia, to Ohio Valley, all the way to Maine.
"The Big Snow of 1836" January 8–10, 1836. Produced 30 inches (76 cm) to 40 inches (100 cm) of snowfall in interior New York, northern Pennsylvania, and western New England. Philadelphia got a reported 15 inches (38 cm) and New York City 2 feet (61 cm) of snow.

1851 to 1900
Plains Blizzard of 1856. December 3–5, 1856. Severe blizzard-like storm raged for three days in Kansas and Iowa. Early pioneers suffered.
"The Cold Storm of 1857" January 18–19, 1857. Produced severe blizzard conditions from North Carolina to Maine. Heavy snowfalls reported in east coast cities.
Midwest Blizzard of 1864. January 1, 1864. Gale-force winds, driving snow, and low temperatures all struck simultaneously around Chicago, Wisconsin and Minnesota.
Plains Blizzard of 1873. January 7, 1873. Severe blizzard struck the Great Plains. Many pioneers from the east were unprepared for the storm and perished in Minnesota and Iowa.
Great Plains Easter Blizzard of 1873. April 13, 1873
Seattle Blizzard of 1880. January 6, 1880. Seattle areas greatest snowstorm to date. An estimated 4 feet (120 cm) fell around the town. Many barns collapsed and all transportation halted.
The Snow Winter of 1880–1881. Laura Ingalls Wilders book The Long Winter details the effects of the blizzards in the Dakota Territory in  the winter of 1880–1881.
In the three year winter period from December 1885 to March 1888, the Great Plains and Eastern United States suffered a series of the worst blizzards in this nations history ending with the Schoolhouse Blizzard and the Great Blizzard of 1888. The massive explosion of the volcano Krakatoa in the South Pacific late in August 1883 is a suspected cause of these huge blizzards during these several years. The clouds of ash it emitted continued to circulate around the world for many years. Weather patterns continued to be chaotic for years, and temperatures did not return to normal until 1888. Record rainfall was experienced in Southern California during July 1883 to June 1884. The Krakatoa eruption injected an unusually large amount of sulfur dioxide (SO2) gas high into the stratosphere which reflects sunlight and helped cool the planet over the next few years until the suspended atmospheric sulfur fell to ground.
Plains Blizzard of late 1885. In Kansas, heavy snows of late 1885 had piled drifts 10 feet (3.0 m) high.
Kansas Blizzard of 1886. First week of January 1886. Reported that 80 percent of the cattle were frozen to death in that state alone from the cold and snow.
January 1886 Blizzard. January 9, 1886. Same system as Kansas 1886 Blizzard that traveled eastward.
Great Plains Blizzards of late 1886. On November 13, 1886, it reportedly began to snow and did not stop for a month in the Great Plains region.
Great Plains Blizzard of 1887. January 9–11, 1887. Reported 72-hour blizzard that covered parts of the Great Plains in more than 16 inches (41 cm) of snow. Winds whipped and temperatures dropped to around 50 °F (10 °C). So many cows that were not killed by the cold soon died from starvation. When spring arrived, millions of the animals were dead, with around 90 percent of the open ranges cattle rotting where they fell. Those present reported carcasses as far as the eye could see. Dead cattle clogged up rivers and spoiled drinking water. Many ranchers went bankrupt and others simply called it quits and moved back east. The "Great Die-Up" from the blizzard effectively concluded the romantic period of the great Plains cattle drives.
Schoolhouse Blizzard of 1888 North American Great Plains. January 12–13, 1888. What made the storm so deadly was the timing (during work and school hours), the suddenness, and the brief spell of warmer weather that preceded it. In addition, the very strong wind fields behind the cold front and the powdery nature of the snow reduced visibilities on the open plains to zero. People ventured from the safety of their homes to do chores, go to town, attend school, or simply enjoy the relative warmth of the day. As a result, thousands of people—including many schoolchildren—got caught in the blizzard.
Great Blizzard of March 1888 March 11–14, 1888. One of the most severe recorded blizzards in the history of the United States. On March 12, an unexpected northeaster hit New England and the mid-Atlantic, dropping up to 50 in (130 cm) of snow in the space of three days. New York City experienced its heaviest snowfall recorded to date at that time, all street railcars were stranded, and the storm led to the creation of the NYC subway system. Snowdrifts reached up to the second story of some buildings. Some 400 people died from this blizzard, including many sailors aboard vessels that were beset by gale-force winds and turbulent seas.
Great Blizzard of 1899 February 11–14, 1899. An extremely unusual blizzard in that it reached into the far southern states of the US. It hit in February, and the area around Washington, D.C., experienced 51 hours straight of snowfall. The port of New Orleans was totally iced over; revelers participating in the New Orleans Mardi Gras had to wait for the parade routes to be shoveled free of snow. Concurrent with this blizzard was the extremely cold arctic air. Many city and state record low temperatures date back to this event, including all-time records for locations in the Midwest and South. State record lows: Nebraska reached −47 °F (−44 °C), Ohio experienced −39 °F (−39 °C), Louisiana bottomed out at −16 °F (−27 °C), and Florida dipped below zero to −2 °F (−19 °C).

1901 to 1939
Great Lakes Storm of 1913 November 7–10, 1913. “The White Hurricane” of 1913 was the deadliest and most destructive natural disaster ever to hit the Great Lakes Basin in the Midwestern United States and the Canadian province of Ontario. It produced 90 mph (140 km/h) wind gusts, waves over 35 ft (11 m) high, and whiteout snowsqualls. It killed more than 250 people, destroyed 19 ships, and stranded 19 others.
Blizzard of 1918. January 11, 1918. Vast blizzard-like storm moved through Great Lakes and Ohio Valley.
1920 North Dakota blizzard March 15–18, 1920
Knickerbocker Storm January 27–28, 1922

1940 to 1949
Armistice Day Blizzard of 1940 November 10–12, 1940. Took place in the Midwest region of the United States on Armistice Day. This "Panhandle hook" winter storm cut a 1,000 mi-wide path (1,600 km) through the middle of the country from Kansas to Michigan. The morning of the storm was unseasonably warm but by mid afternoon conditions quickly deteriorated into a raging blizzard that would last into the next day. A total of 145 deaths were blamed on the storm, almost a third of them duck hunters who had taken time off to take advantage of the ideal hunting conditions. Weather forecasters had not predicted the severity of the oncoming storm, and as a result the hunters were not dressed for cold weather. When the storm began many hunters took shelter on small islands in the Mississippi River, and the 50 mph (80 km/h) winds and 5-foot (1.5 m) waves overcame their encampments. Some became stranded on the islands and then froze to death in the single-digit temperatures that moved in over night. Others tried to make it to shore and drowned.
North American blizzard of 1947 December 25–26, 1947. Was a record-breaking snowfall that began on Christmas Day and brought the Northeast United States to a standstill. Central Park in New York City got 26 inches (66 cm) of snowfall in 24 hours with deeper snows in suburbs. It was not accompanied by high winds, but the snow fell steadily with drifts reaching 10 ft (3.0 m). Seventy-seven deaths were attributed to the blizzard.
The Blizzard of 1949 - The first blizzard started on Sunday, January 2, 1949; it lasted for three days. It was followed by two more months of blizzard after blizzard with high winds and bitter cold. Deep drifts isolated southeast Wyoming, northern Colorado, western South Dakota and western Nebraska, for weeks. Railroad tracks and roads were all drifted in with drifts of 20 feet (6.1 m) and more.  Hundreds of people that had been traveling on trains were stranded.  Motorists that had set out on January 2 found their way to private farm homes in rural areas and hotels and other buildings in towns; some dwellings were so crowded that there wasnt enough room for all to sleep at once.  It would be weeks before they were plowed out. The Federal government quickly responded with aid, airlifting food and hay for livestock.  The total rescue effort involved numerous volunteers and local agencies plus at least ten major state and federal agencies from the U.S. Army to the National Park Service. Private businesses, including railroad and oil companies, also lent manpower and heavy equipment to the work of plowing out. The official death toll was 76 people and one million livestock. Youtube video  Storm of the Century - the Blizzard of  49 Storm of the Century - the Blizzard of 49

1950 to 1959
Great Appalachian Storm of November 1950 November 24–30, 1950
March 1958 Noreaster blizzard March 18–21, 1958.
The Mount Shasta California Snowstorm of 1959 – The storm dumped 189 inches (480 cm) of snow on Mount Shasta. The bulk of the snow fell on unpopulated mountainous areas, barely disrupting the residents of the Mount Shasta area. The amount of snow recorded is the largest snowfall from a single storm in North America.

1960 to 1969
March 1960 Noreaster blizzard March 2–5, 1960
December 1960 Noreaster blizzard December 12–14, 1960. Wind gusts up to 50 miles per hour (80 km/h).
March 1962 Noreaster Great March Storm of 1962 – Ash Wednesday. North Carolina and Virginia blizzards. Struck during Spring high tide season and remained mostly stationary for almost 5 days causing significant damage along eastern coast, Assateague island was under water, and dumped 42 inches (110 cm) of snow in Virginia.
North American blizzard of 1966 January 27–31, 1966
Chicago Blizzard of 1967 January 26–27, 1967
February 1969 noreaster February 8–10, 1969
March 1969 Noreaster blizzard March 9, 1969
December 1969 Noreaster blizzard December 25–28, 1969.

1970 to 1979
The Great Storm of 1975 known as the "Super Bowl Blizzard" or "Minnesotas Storm of the Century". January 9–12, 1975. Wind chills of −50 °F (−46 °C) to −80 °F (−62 °C) recorded, deep snowfalls.
Groundhog Day gale of 1976 February 2, 1976
Buffalo Blizzard of 1977 January 28 – February 1, 1977. There were several feet of packed snow already on the ground, and the blizzard brought with it enough snow to reach Buffalos record for the most snow in one season – 199.4 inches (506 cm).
Great Blizzard of 1978 also called the "Cleveland Superbomb". January 25–27, 1978. Was one of the worst snowstorms the Midwest has ever seen. Wind gusts approached 100 mph (160 km/h), causing snowdrifts to reach heights of 25 ft (7.6 m) in some areas, making roadways impassable. Storm reached maximum intensity over southern Ontario Canada.
Northeastern United States Blizzard of 1978 – February 6–7, 1978. Just one week following the Cleveland Superbomb blizzard, New England was hit with its most severe blizzard in 90 years since 1888.
Chicago Blizzard of 1979 January 13–14, 1979

1980 to 1989
February 1987 Noreaster blizzard February 22–24, 1987

1990 to 1999
1991 Halloween blizzard Upper Mid-West US, October 31 – November 3, 1991
December 1992 Noreaster blizzard December 10–12, 1992
1993 Storm of the Century March 12–15, 1993. While the southern and eastern U.S </s>


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