<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 Tungiasis and explain in detail? [/INST] Tungiasis  is an inflammatory skin disease caused by infection with the female ectoparasitic Tunga penetrans, a flea also known as the chigoe, chigo, chigoe flea, chigo flea, jigger, nigua, sand flea, or burrowing flea (and not to be confused with the chigger, a different arthropod). The flea and the disease that it causes are found in the tropical parts of Africa, the Caribbean, Central and South America, and India. Tunga penetrans is the smallest known flea, measuring 1 mm across. It is also known in Latin America as the nigua and bicho de pie (Spanish) or bicho de pé (Portuguese), literally "foot bug". Tunga penetrans is a member of the genus Tunga, which comprises 13 species.Tungiasis causes skin inflammation, severe pain, itching, and a lesion at the site of infection that is characterized by a black dot at the center of a swollen red lesion, surrounded by what looks like a white halo. Desquamation of the skin is always seen, especially after the flea expands during hypertrophy.
As of 2009, tungiasis is present worldwide in 88 countries with varying degrees of incidence.  This disease is of special public health concern in highly endemic areas such as Nigeria, Trinidad and Tobago, and Brazil, where its prevalence, especially in poor communities, has been known to approach 50%.The chigoe flea is properly classified as a member of the order Siphonaptera as it is a flea. Although commonly referred to as chiggers, true chiggers are mites, which are minute arachnids. Mites penetrate the skin and feed on skin cells that are broken down by an enzyme they secrete from their mouthparts, but they do not lay eggs in the host as T. penetrans does. Moreover, in mites, the adult and the larval forms both feed on other animals. This is not the case with T. penetrans, as only the adults feed on mammals and it is only the female that stays attached to the host.
Tunga penetrans is also known by the following names: chigoe flea, sand flea, nigua, chigger flea, jigger flea, bicho de pé, pico, sikka, kuti, and piqui, among many others.

Signs and symptoms
The symptoms of this disease include:
Severe pruritus
Pain
Inflammation and swelling
Lesions and ulcerations, with black dots in the centerIf a Tunga infection is left untreated, secondary infections, such as bacteremia, tetanus, necrosis and gangrene, may be expected.
In all cases, tungiasis by itself only caused morbidity, though secondary infection may lead to mortality. The life cycle section presents the Fortaleza stages from the fleas developmental perspective. The discussion is specific to symptoms of human infection. The clinical presentation in humans follows the Fortaleza Classification as the stage of infection will determine the symptoms present. The following discussion will give an overview of the symptoms beginning in stage 2 because patients are not likely to present themselves at the early stages of infection, mostly because the fleas burrowing is usually not felt. This may be due to a keratolytic enzyme secreted during stage 1.The patient with a single flea may present as early as stage 2 when, though the erythema is barely perceptible, a boring pain and the curious sensation of pleasant itching occur. This inflammatory reaction is the initial immunological response to the infestation. Heavily infested patients may not notice a stage 2 infection due to the other fleas’ causing irritation as well. Feces may be seen, but this is more common in the 3rd stage.
Around the third day after penetration, erythema and skin tenderness are felt, accompanied by pruritus (severe itching) and a black furuncular nodule surrounded by a white halo of stretched skin caused by the expansion of the flea. Fecal coils may protrude from the center of the nodule where the fleas anus is facing upward. They should be washed off quickly as the feces may remain in the skin unless removed. During this 3a substage, pain can be severe, especially at night or, if the nodule is on the foot, while walking. Eggs will also begin to be released and a watery secretion can be observed. The radical metamorphosis during the 3rd to 6th day after penetration, or neosomy, precedes the formation of a small caldera-like rim rampart as a result of the increased thickness of the fleas chitin exoskeleton. During the caldera formation, the nodule shrinks a bit and it looks as if it is beginning to dry out; this takes 2 weeks and comprises substage 3b.At the third week after penetration and substage 4a, the eggs’ release will have stopped and the lesion will become smaller and more wrinkled. As the flea is near death, fecal and water secretion will stop altogether. Pain, tenderness, and skin inflammation will still be present. Around the 25th day after penetration, the lesion looks like a black crust and the fleas carcass is removed by host repair mechanisms and the skin begins to heal. With the flea gone, inflammation may still persist for a while.Although patients would not present within the 5th stage of tungiasis as the flea would be dead and no longer in the body, this stage is characterized by the reorganization of the skin (1–4 weeks) and a circular residue of 5–10 mm in diameter around the site in penetration. An intraepithelial abscess, which developed due to the presence of the flea, will drain and later heal.  Although these disease residues would persist for a few months, tungiasis is no longer present.In severe cases, ulcers are common, as well as complete tissue and nail deformation. A patient may be unable to walk due to severe pain if too many of the lesions are present in the feet. Suppuration (pus formation), tissue death, auto-amputation of digits (via ainhum), and chronic lymphedema may also be seen.If the patient is not vaccinated, tetanus is often a complication due to secondary infection. Necrosis and gangrene are other common complications of severe infestation and superinfection. Staphylococcus aureus and Wolbachia endobacteria can be transmitted by the chigoe flea, as well as nearly 150 other different pathogens. For these reasons, the chigoe flea should be removed as soon as possible.

Incubation
Because of the relatively rapid onset of tungiasis, the incubation period tends to be short. Although some reddening around the site of penetration occurs, the first symptoms are perceived in stage 2 as itching and severe pain, usually a day after penetration.

Cause
Tungiasis is strictly caused by chigoe fleas (the term transmission does not apply because Tunga penetrans is itself responsible for the disease.) The preponderance of tungiasis lesions on the toes may be because chigoe flea is a poor jumper, attaining only a high of 20 cm. But the reality is more complex; for example, the jumping ability cannot explain why hands are the second-most affected body part. Lesions on the hands are better explained by playing in the sand and noting that hands are often used to remove sand from other parts of the body. The occurrence of tungiasis lesions on the toes, between them, and on the soles can be easily explained because most of the victims are poor, walk barefoot, and live in places where the sand (home to chigoe fleas) constitutes the floor. Rate of incidence therefore is greatly increased in poor communities and populations because of the lack of adequate housing.  This occurs in significantly higher proportions during the peak of the dry season in local communities.

Reservoirs and transmission
T. penetrans has been documented to use various warm-blooded animals as reservoir hosts, including humans, pigs, dogs, cats, rats, sheep, cattle, donkeys, monkeys, birds, and elephants. These hosts directly propagate the disease by being the origin of the next generation of fleas. Once the female flea expels 100–200 eggs, the cycle of transmission begins again.

Lifecycle
T. penetrans eggs, on average, are 604 μm long, The larva will hatch from the egg within one to six days, assuming the environmental conditions (e.g., moisture, humidity, etc.) are favorable. After hatching, the flea will progress through two instar phases. This is unique in that most fleas go through three, instead. Over the course of that development, the flea will first decrease in size from its just-hatched size of 1,500 μm to 1,150 μm (first instar) before growing to 2,900 μm (second instar).About 6 to 8 days after hatching, the larva pupates and builds a cocoon around itself. Because it lives mostly on and below the surface of the sand, sand is used to stabilize the cocoon and help to promote its development. An environmental disturbance such as rain or a lack of sand have been shown to decrease incidence, most likely due to decreasing the environmental factors (i.e., sand) on which the flea depends for overall growth. Barring any disturbances to the cocoon, an adult flea will emerge from the puparium after 9–15 days.In the adult phase, the flea will occasionally feed on unsuspecting animals. Only once the female burrows into the skin can reproduction occur, as the male and female show no interest in each other in the wild. The male flea dies after copulation. The female flea continues in vivo ectodevelopment, described in stages by the Fortaleza classification of tungiasis.

Fortaleza classification
In a seminal paper on the biology and pathology of Tunga penetrans, Eisele et al. (2003) provided and detailed the five stages of tungiasis, thereby detailing the in vivo development of the female chigoe flea for the first time. In dividing the natural history of the disease, the Fortaleza Classification formally describes the last part of the female fleas life cycle where it burrows into its hosts skin, expels eggs, and dies. Due to the nature of the discussion, overlap with other sections, particularly the one on symptoms, is unavoidable.Stage 1 is characterized by the penetration of the skin by the female chigoe flea. Running along the body, the female uses its posterior legs to push its body upward by an angle of 45–90 degrees. Penetration then starts, beginning with the proboscis going through the epidermis.By stage 2 (day 1–2), penetration is complete and the flea has burrowed most of its body into the skin. Only the anus, the copulatory organs, and four rear air holes in fleas called stigmata remain on the outside of the epidermis. The anus will excrete feces that is thought to attract male fleas for mating, described in a later section. The hypertrophic zone between tergites 2 and 3 in the abdominal region begins to expand a day or two after penetration and takes the appearance of a life belt. During this time, the flea begins to feed on the hosts blood.Stage 3 is divided into two substages, 3a and 3b. Stage 3a is 2–3 days after penetration is complete. In substage 3a, the fleas midsection swells, balloon-like, to the size of a pea. This expansion of the flea causes its integument to be stretched thin, a process called physogastrism. The swelling ends in the condition of physogastry, and results in the appearance of a white halo around a black dot at the center of the lesion. That dot is the rear end of the flea. In substage 3b, the chitin exoskeleton of tergites 2 and 3 increase in thickness, which gives the structure the look of a miniature caldera. Egg release is common in substage 3b, as are fecal coils. The eggs tend to stick to the skin.At about the 3rd week after penetration, stage 4 begins, which is also divided into two substages. In 4a, the flea loses its signs of vitality and appears near death. As a result, the lesion shrinks in size, turns brown, and appears wrinkled. The death of the flea marks the beginning of substage 4b (around day 25 post-penetration) as the body begins to eliminate the parasite through skin repair mechanisms (e.g. shedding and subsequent skin repair). At this phase, the lesion is seen as brown or black.By the 5th stage of tungiasis, the carcass of the T. penetrans flea has been expelled and there are circular skin residues of the infection that remain. There are only lingering symptoms at this time, described in the next section.

Morphology
In a study of 1000 freshly ejected T. penetrans eggs, it was found that females are generally smaller than males for all criteria. In some cases, though, females had a bigger epipharynx and maxillar palpus. Due to its burrowing activity, the chigoe flea has developed a well-developed lacinia and epipharynx that is used to penetrate the skin. Overall, the fleas’ head is relatively flattened, which again aids in burrowing through the epidermal and dermal layers.Investigators have also found that adult T. penetrans have different morphologies with respect to the shape of their head. Some have a rounded head, others have head shapes that resemble ski ramps more than anything else; still, others demonstrate head shapes that are very linear with a slight bulge at the nose. These morphologies were seen to be host-specific, as only fleas of some head-types were found in specific hosts. This, along with genetic differences among the T. penetrans fleas that infect different host animals, may suggest that there are several species of closely related species have been grouped taxonomically under one binomial nomenclature.Though the chigoe flea resembles most others in morphology, the flea has a hypertrophic region between tergites 2 and 3. As stated in Eisele et al. (2003), tergites 2 and 3, as well as the abdominal sternites, stretch considerably and are bent apart. Chitinous clasps that are built for the abdominal enlargement surround these regions and hold onto the hypertrophic zone, giving them the appearance of a three-leafed clover. (See image 7 of the life cycle diagram.) Surprisingly, the rest of the flea, including the head and the thorax, do not change in shape.,With the rapid expansion of the flea, the morphology of the flea is now vastly different. It has gone from the smallest flea in the world to a bulging mass that measures 5–10mm in diameter. This results in a volume that is 2000 to 3000 times what it used to be.

Reproduction
Females have a depression or groove at their abdominal end whereas the males have their protrusive copulatory organs in that same region. These morphological differences reflect the way the male and female copulate. In the first step toward copulation, the female penetrates an organism in an ungravid state. It is only there that the male will find her and copulate. Copulation of adults has not been observed in the wild. With the female reproductive organs pointing outward, the male will place his reproductive organs "in direction to the upright abdominal end of the female" to copulate. Having copulated for only a few seconds to 2 minutes, the male will then begin to search for another female. After copulation is complete, the male will die, although sometimes he will take a blood meal before doing so. Eggs will be expelled whether or not they have been fertilized.The chigoe flea eggs’ average length is 604 μm and the just hatched larvae, in their first instar, have an average length of 1,500 μm. At the second and last instar (T. penetrans is unique among the fleas in that it only has two, instead of three, instars.) the larvae decrease in size to 1,150 μm after growing to at least 2,900 μm. The development from instar 1 to instar 2 lasts less than one day.On the whole, Tunga penetrans does not do very well in terms of its Darwinian fitness. In a laboratory setting in which different mediums were provided for larval growth, the rate of survival from egg to adult in the best medium was 1.05%. Only 15% of the eggs were found to develop into larvae, and of those, only 14% formed a cocoon. Moreover, only half of the pupae reached the adult phase, resulting in gender disequilibrium. Although these results reflect a laboratory setting, the general lack of success for T. penetrans’s reproductive (opportunistic) R-strategy is surprising given the number of fleas that a single person can attract. The low survival rate suggests that a concentrated public health effort directed at any point in the flea’s life cycle is likely to deal a crippling blow to the overall population of the flea in the area.

Diagnosis
There are no diagnostic tests for tungiasis. This is most likely because the parasite is ectoparasitic with visible symptoms. Identification of the parasite through removal, and a patient’s traveling history, should suffice for diagnosis, though the latter is clearly more useful than the former. Localization of the lesion may be a useful diagnostic method for the clinician. A biopsy may be done, though again, it is not required for diagnosis.

Prevention
Due to the high number of hosts, eradication of tungiasis is not feasible, at least not easily so. Public health and prevention strategies should then be done with elimination as the target. Better household hygiene, including having a cemented rather than a sand floor, and washing it often, would lower the rates of tungiasis significantly.Though vaccines would be useful, due to the ectoparasitic nature of chigoe flea, they are neither a feasible nor an effective tool against tungiasis. Nevertheless, due to the high incidence of secondary infection, those at risk of tungiasis should get vaccinated against tetanus. A better approach is to use repellents that specifically target the chigoe flea. One very successful repellent is called Zanzarin, a derivative of coconut oil, jojoba oil, and aloe vera. In a recent study involving two cohorts, the infestation rates dropped 92% on average for the first one and 90% for the other. Likewise, the intensity of the cohorts dropped by 86% and 87% respectively. The non-toxic nature of Zanzarin, combined with its "remarkable regression of the clinical pathology" make this a tenable public health tool against tungiasis.The use of pesticide, like DDT, has also led to elimination of the Tunga penetrans, but this control/prevention strategy should be utilized very carefully, if at all, because of the possible side effects such pesticides can have on the greater biosphere. In the 1950s, there was a worldwide effort to eradicate malaria. As part of that effort, Mexico launched the Campaña Nacional para la Erradicación de Paludismo, or the National Campaign for the Eradication of Malaria. By spraying DDT in homes, the Anopheles a genus of mosquitoes known to carry the deadly Plasmodium falciparum was mostly eliminated. As a consequence of this national campaign, other arthropods were either eliminated or significantly reduced in number, including the reduviid bug responsible for Chagas disease (American Trypanosomiasis) and T. penetrans. Controlled, in-home spraying of DDT is effective as it gives the home immunity against arthropods while not contaminating the local water supplies and doing as much ecological damage as was once the case when DDT was first introduced.While other species gradually gained resistance to DDT and other insecticides that were used, T. penetrans did not; as a result, the incidence of tungiasis in Mexico is very low when compared to the rest of Latin America, especially Brazil, where rates in poor areas have been known to be as high or higher than 50%. There was a 40-year period with no tungiasis cases in Mexico. It was not until August 1989 that three Mexican patients presented with the disease. Though there were other cases of tungiasis reported thereafter, all were acquired in Africa.

Treatment
As the disease is self-limiting, at least when exposure to the parasite is limited, management is mostly confined to treatment. Due to the secondary infection that can cause serious medical issues, the recommended course of action upon diagnosis is a surgical extraction of the fleas followed by the application of a topical antibiotic. Care should be taken to avoid tearing the flea during the extraction procedures as severe inflammation will result. The same will occur if part of the flea is left behind. Sterile equipment should always be used, as contaminated instruments could act as mechanical vectors for pathogens to enter the body.There is no drug that has proven to be effective against embedded fleas. Oral niridazole was once considered a therapeutic drug, but well-designed studies are lacking and, given the severe adverse effects, this is one drug that is likely to cause more harm than good. However, it has some anecdotal evidence of lysing the fleas altogether. Oral ivermectin is considered by some in endemic areas to be a panacea against the fleas but studies using high doses have failed to validate this hypothesis. Other drugs such as topical ivermectin and metrifonate have been somewhat successful, but not enough to be significant. [2,5] For superinfections, trimethoprim, sulfamethoxazole, metronidazole, amoxicillin, (with/without clavulanate) have been used successfully, though these treat only secondary infections.Successful topical treatments also include cryotherapy and electrodesiccation of the lesion. If formaldehyde, chloroform, or DDT are used topically, care should be taken when dealing with the resulting morbidity. The T. penetrans flea can also be suffocated using occlusive petrolatum, while Vaseline will kill the organism as well, most likely due to suffocation as the stigmata would be covered. The gum of the mammee apple (Mammea americana), a fruit that also goes by the name Saint Domingo apricot, has also been used to kill the chigoe flea, though this has not been reported in the main T. penetrans literature.Even without treatment, the burrowed fleas will die within five weeks and are naturally sloughed off as the skin sheds.

Epidemiology
For the most part, the chigoe flea lives 2–5 cm below the sand, an observation which helps explains its overall distribution. The temperature is generally too hot for the larvae to develop on the surface of the sand and the deeper sand does not have enough oxygen. This preferred ecological niche offers a way to decrease transmission among humans by investing in concrete grounds as opposed to the sand that is usually used in shacks and some favelas. Indeed, Nany et al. (2007) report that "In shacks with concreted ground being cleaned every day with water, Tunga [penetrans] larvae were hardly found."In a longitudinal study conducted from March 2001 to January 2002, incidence of tungiasis was found to vary significantly with the local seasons of an endemic community in Brazil. In particular, the study found that "occurrence of tungiasis varies throughout the year and seems to follow local precipitation patterns. Maximum and minimum prevalence rates differed by more than a factor of three." The authors suggest that the correlation is due to the high humidity in the soil impairing larval development during the rainy season, as well as the more obvious reason that rain may simply wash away all stages of T. penetrans due its small size of 1mm.Acting as both biological vectors and definitive hosts, humans have spread Tunga penetrans from its isolated existence in the West Indies to all of Latin America and most of Africa via sea travel. Since the chigoe flea technically has no reservoir species and the female will cause tungiasis to any mammalian organism it can penetrate, this means the flea will have a relatively large number of hosts and victims </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 II and explain in detail? [/INST]  </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 Multiple abnormalities and explain in detail? [/INST]  </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 Arm and explain in detail? [/INST] In human anatomy, the arm refers to the upper limb in common usage, although academically the term specifically means the upper arm between the glenohumeral joint (shoulder joint) and the elbow joint. The distal part of the upper limb between the elbow and the radiocarpal joint (wrist joint) is known as the forearm or "lower" arm, and the extremity beyond the wrist is the hand.
By anatomical definitions, the bones, ligaments and skeletal muscles of the shoulder girdle, as well as the axilla between them, is considered parts of the upper limb, and thus also components of the arm. The Latin term brachium, which serves as a root word for naming many anatomical structures, may refer to either the upper limb as a whole or to the upper arm on its own.

Anatomy
Bones
The humerus is one of the three long bones of the arm. It joins with the scapula at the shoulder joint and with the other long bones of the arm, the ulna and radius at the elbow joint. The elbow is a complex hinge joint between the end of the humerus and the ends of the radius and ulna.

Muscles
The arm is divided by a fascial layer (known as lateral and medial intermuscular septa) separating the muscles into two osteofascial compartments: the anterior and the posterior compartments of the arm. The fascia merges with the periosteum (outer bone layer) of the humerus.The anterior compartment contains three muscles: biceps brachii, brachialis and coracobrachialis muscles. They are all innervated by the musculocutaneous nerve. The posterior compartment contains only the triceps brachii muscle, supplied by the radial nerve.

Nerve supply
The musculocutaneous nerve, from C5, C6, C7, is the main supplier of muscles of the anterior compartment. It originates from the lateral cord of the brachial plexus of nerves. It pierces the coracobrachialis muscle and gives off branches to the muscle, as well as to brachialis and biceps brachii. It terminates as the anterior cutaneous nerve of the forearm.
The radial nerve, which is from the fifth cervical spinal nerve to the first thoracic spinal nerve, originates as the continuation of the posterior cord of the brachial plexus. This nerve enters the lower triangular space (an imaginary space bounded by, amongst others, the shaft of the humerus and the triceps brachii) of the arm and lies deep to the triceps brachii. Here it travels with the deep artery of the arm, which sits in the radial groove of the humerus. This fact is very important clinically as a fracture of the shaft of the bone here can cause lesions or even transections in the nerve.
Other nerves passing through give no supply to the arm. These include:

The median nerve, nerve origin C5-T1, which is a branch of the lateral and medial cords of the brachial plexus. This nerve continues in the arm, travelling in a plane between the biceps and triceps muscles. At the cubital fossa, this nerve is deep to the pronator teres muscle and is the most medial structure in the fossa. The nerve passes into the forearm.
The ulnar nerve, origin C8-T1, is a continuation of the medial cord of the brachial plexus. This nerve passes in the same plane as the median nerve, between the biceps and triceps muscles. At the elbow, this nerve travels posterior to the medial epicondyle of the humerus. This means that condylar fractures can cause lesion to this nerve.

Blood supply
The main artery in the arm is the brachial artery. This artery is a continuation of the axillary artery. The point at which the axillary becomes the brachial is distal to the lower border of teres major. The brachial artery gives off an unimportant branch, the deep artery of arm. This branching occurs just below the lower border of teres major.
The brachial artery continues to the cubital fossa in the anterior compartment of the arm. It travels in a plane between the biceps and triceps muscles, the same as the median nerve and basilic vein. It is accompanied by venae comitantes (accompanying veins). It gives branches to the muscles of the anterior compartment. The artery is in between the median nerve and the tendon of the biceps muscle in the cubital fossa. It then continues into the forearm.
The deep artery of the arm travels through the lower triangular space with the radial nerve. From here onwards it has an intimate relationship with the radial nerve. They are both found deep to the triceps muscle and are located on the spiral groove of the humerus. Therefore, fracture of the bone may not only lead to lesion of the radial nerve, but also haematoma of the internal structures of the arm. The artery then continues on to anastamose with the recurrent radial branch of the brachial artery, providing a diffuse blood supply for the elbow joint.

Veins
The veins of the arm carry blood from the extremities of the limb, as well as drain the arm itself </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 Borderline intellectual functioning and explain in detail? [/INST] Borderline intellectual functioning, also called borderline mental retardation (in the ICD-8), is a categorization of intelligence wherein a person has below average cognitive ability (generally an IQ of 70–85), but the deficit is not as severe as intellectual disability (below 70). It is sometimes called below average IQ (BAIQ). This is technically a cognitive impairment; however, this group may not be sufficiently mentally disabled to be eligible for specialized services.

Codes
The DSM-IV-TR code of borderline intellectual functioning is V62.89. DSM-5 diagnosis codes are V62.89 and R41.83.

Learning skills
During school years, individuals with borderline intellectual functioning are often "slow learners" </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 Delusion and explain in detail? [/INST] A delusion is a false fixed belief that is not amenable to change in light of conflicting evidence. As a pathology, it is distinct from a belief based on false or incomplete information, confabulation, dogma, illusion, hallucination, or some other misleading effects of perception, as individuals with those beliefs are able to change or readjust their beliefs upon reviewing the evidence. However:
"The distinction between a delusion and a strongly held idea is sometimes difficult to make and depends in part on the degree of conviction with which the belief is held despite clear or reasonable contradictory evidence regarding its veracity."Delusions have been found to occur in the context of many pathological states (both general physical and mental) and are of particular diagnostic importance in psychotic disorders including schizophrenia, paraphrenia, manic episodes of bipolar disorder, and psychotic depression.

Types
Delusions are categorized into four different groups:

Bizarre delusion: Delusions are deemed bizarre if they are clearly implausible and not understandable to same-culture peers and do not derive from ordinary life experiences. An example named by the DSM-5 is a belief that someone replaced all of ones internal organs with someone elses without leaving a scar, depending on the organ in question.
Non-bizarre delusion: A delusion that, though false, is at least technically possible, e.g., the affected person mistakenly believes that they are under constant police surveillance.
Mood-congruent delusion: Any delusion with content consistent with either a depressive or manic state, e.g., a depressed person believes that news anchors on television highly disapprove of them, or a person in a manic state might believe they are a powerful deity.
Mood-neutral delusion: A delusion that does not relate to the patients emotional state; for example, a belief that an extra limb is growing out of the back of ones head is neutral to either depression or mania.

Themes
In addition to these categories, delusions often manifest according to a consistent theme. Although delusions can have any theme, certain themes are more common. Some of the more common delusion themes are:

Delusion of control: False belief that another person, group of people, or external force controls ones general thoughts, feelings, impulses, or behaviors.
Cotard delusion: False belief that one does not exist or that one has died. Some cases also include the belief that one is immortal or that one has lost their internal organs, blood, or other body parts.
Delusional jealousy: False belief that a spouse or lover is having an affair, with no proof to back up the claim.
Delusion of guilt or sin (or delusion of self-accusation): Ungrounded feeling of remorse or guilt of delusional intensity.
Delusion of mind being read: False belief that other people can know ones thoughts.
Delusion of thought insertion: Belief that another thinks through the mind of the person.
Delusion of reference: False belief that insignificant remarks, events, or objects in ones environment have personal meaning or significance. "Usually the meaning assigned to these events is negative, but the messages can also have a grandiose quality."
Erotomania: False belief that another person is in love with them.
Religious delusion: Belief that the affected person is a god or chosen to act as a god.
Somatic delusion: Delusion whose content pertains to bodily functioning, bodily sensations or physical appearance. Usually the false belief is that the body is somehow diseased, abnormal or changed. A specific example of this delusion is delusional parasitosis: Delusion in which one feels infested with insects, bacteria, mites, spiders, lice, fleas, worms, or other organisms.
Delusion of poverty: Person strongly believes they are financially incapacitated. Although this type of delusion is less common now, it was particularly widespread in the days preceding state support.

Grandiose delusions
Grandiose delusions or delusions of grandeur are principally a subtype of delusional disorder but could possibly feature as a symptom of schizophrenia and manic episodes of bipolar disorder. Grandiose delusions are characterized by fantastical beliefs that one is famous, omnipotent or otherwise very powerful. The delusions are generally fantastic, often with a supernatural, science-fictional, or religious bent. In colloquial usage, one who overestimates ones own abilities, talents, stature or situation is sometimes said to have "delusions of grandeur". This is generally due to excessive pride, rather than any actual delusions. Grandiose delusions or delusions of grandeur can also be associated with megalomania.

Persecutory delusions
Persecutory delusions are the most common type of delusions and involve the theme of being followed, harassed, cheated, poisoned or drugged, conspired against, spied on, attacked, or otherwise obstructed in the pursuit of goals.
Persecutory delusions are a condition in which the affected person wrongly believes that they are being persecuted. Specifically, they have been defined as containing two central elements: The individual thinks that:

harm is occurring, or is going to occur
the persecutors have the intention to cause harmAccording to the DSM-IV-TR, persecutory delusions are the most common form of delusions in schizophrenia, where the person believes they are "being tormented, followed, sabotaged, tricked, spied on, or ridiculed". In the DSM-IV-TR, persecutory delusions are the main feature of the persecutory type of delusional disorder. When the focus is to remedy some injustice by legal action, they are sometimes called "querulous paranoia".

Causes
Explaining the causes of delusions continues to be challenging and several theories have been developed. One is the genetic or biological theory, which states that close relatives of people with delusional disorder are at increased risk of delusional traits. Another theory is the dysfunctional cognitive processing, which states that delusions may arise from distorted ways people have of explaining life to themselves. A third theory is called motivated or defensive delusions. This one states that some of those persons who are predisposed might experience the onset of delusional disorder in those moments when coping with life and maintaining high self-esteem becomes a significant challenge. In this case, the person views others as the cause of their personal difficulties in order to preserve a positive self-view.This condition is more common among people who have poor hearing or sight. Also, ongoing stressors have been associated with a higher possibility of developing delusions. Examples of such stressors are immigration, low socioeconomic status, and even possibly the accumulation of smaller daily hassles.

Specific delusions
The top two factors mainly concerned in the germination of delusions are disorder of brain functioning and background influences of temperament and personality.Higher levels of dopamine qualify as a symptom of disorders of brain function. That they are needed to sustain certain delusions was examined by a preliminary study on delusional disorder (a psychotic syndrome) instigated to clarify if schizophrenia had a dopamine psychosis. There were positive results - delusions of jealousy and persecution had different levels of dopamine metabolite HVA and homovanillyl alcohol (which may have been genetic). These can be only regarded as tentative results; the study called for future research with a larger population.
It is simplistic to say that a certain measure of dopamine will bring about a specific delusion. Studies show age and gender to be influential and it is most likely that HVA levels change during the life course of some syndromes.On the influence of personality, it has been said: "Jaspers considered there is a subtle change in personality due to the illness itself; and this creates the condition for the development of the delusional atmosphere in which the delusional intuition arises."Cultural factors have "a decisive influence in shaping delusions". For example, delusions of guilt and punishment are frequent in a Western, Christian country like Austria, but not in Pakistan, where it is more likely persecution. Similarly, in a series of case studies, delusions of guilt and punishment were found in Austrian patients with Parkinsons being treated with l-dopa, a dopamine agonist.

Pathophysiology
The two-factor model of delusions posits that dysfunction in both belief formation systems and belief evaluation systems are necessary for delusions. Dysfunction in evaluations systems localized to the right lateral prefrontal cortex, regardless of delusion content, is supported by neuroimaging studies and is congruent with its role in conflict monitoring in healthy persons. Abnormal activation and reduced volume is seen in people with delusions, as well as in disorders associated with delusions such as frontotemporal dementia, psychosis and Lewy body dementia. Furthermore, lesions to this region are associated with "jumping to conclusions", damage to this region is associated with post-stroke delusions, and hypometabolism this region associated with caudate strokes presenting with delusions.The aberrant salience model suggests that delusions are a result of people assigning excessive importance to irrelevant stimuli. In support of this hypothesis, regions normally associated with the salience network demonstrate reduced grey matter in people with delusions, and the neurotransmitter dopamine, which is widely implicated in salience processing, is also widely implicated in psychotic disorders.Specific regions have been associated with specific types of delusions. The volume of the hippocampus and parahippocampus is related to paranoid delusions in Alzheimers disease, and has been reported to be abnormal post mortem in one person with delusions. Capgras delusions have been associated with occipito-temporal damage and may be related to failure to elicit normal emotions or memories in response to faces.

Diagnosis
The modern definition and Jaspers original criteria have been criticised, as counter-examples can be shown for every defining feature.
Studies on psychiatric patients show that delusions vary in intensity and conviction over time, which suggests that certainty and incorrigibility are not necessary components of a delusional belief.Delusions do not necessarily have to be false or incorrect inferences about external reality. Some religious or spiritual beliefs by their nature may not be falsifiable, and hence cannot be described as false or incorrect, no matter whether the person holding these beliefs was diagnosed as delusional or not.
In other situations the delusion may turn out to be true belief. For example, in delusional jealousy, where a person believes that their partner is being unfaithful (and may even follow them into the bathroom believing them to be seeing their lover even during the briefest of partings), it may actually be true that the partner is having sexual relations with another person. In this case, the delusion does not cease to be a delusion because the content later turns out to be verified as true or the partner actually chose to engage in the behavior of which they were being accused.
In other cases, the belief may be mistakenly assumed to be false by a doctor or psychiatrist assessing it, just because it seems to be unlikely, bizarre or held with excessive conviction. Psychiatrists rarely have the time or resources to check the validity of a persons claims leading to some true beliefs to be erroneously classified as delusional. This is known as the Martha Mitchell effect, after the wife of the attorney general who alleged that illegal activity was taking place in the White House. At the time, her claims were thought to be signs of mental illness, and only after the Watergate scandal broke was she proved right (and hence sane).
Similar factors have led to criticisms of Jaspers definition of true delusions as being ultimately un-understandable. Critics (such as R. D. Laing) have argued that this leads to the diagnosis of delusions being based on the subjective understanding of a particular psychiatrist, who may not have access to all the information that might make a belief otherwise interpretable. R. D. Laings hypothesis has been applied to some forms of projective therapy to "fix" a delusional system so that it cannot be altered by the patient. Psychiatric researchers at Yale University, Ohio State University and the Community Mental Health Center of Middle Georgia have used novels and motion picture films as the focus. Texts, plots and cinematography are discussed and the delusions approached tangentially. This use of fiction to decrease the malleability of a delusion was employed in a joint project by science-fiction author Philip Jose Farmer and Yale psychiatrist A. James Giannini. They wrote the novel Red Orcs Rage, which, recursively, deals with delusional adolescents who are treated with a form of projective therapy. In this novels fictional setting other novels written by Farmer are discussed and the characters are symbolically integrated into the delusions of fictional patients. This particular novel was then applied to real-life clinical settings.Another difficulty with the diagnosis of delusions is that almost all of these features can be found in "normal" beliefs. Many religious beliefs hold exactly the same features, yet are not universally considered delusional. For instance, if a person was holding a true belief then they will of course persist with it. This can cause the disorder to be misdiagnosed by psychiatrists. These factors have led the psychiatrist Anthony David to note that "there is no acceptable (rather than accepted) definition of a delusion." In practice, psychiatrists tend to diagnose a belief as delusional if it is either patently bizarre, causing significant distress, or excessively pre-occupying the patient, especially if the person is subsequently unswayed in belief by counter-evidence or reasonable arguments.
Joseph Pierre, M.D. states that one factor that helps differentiate delusions from other kinds of beliefs is that anomalous subjective experiences are often used to justify delusional beliefs. While idiosyncratic and self-referential content often make delusions impossible to share with others, Dr. Pierre suggests that it may be more helpful to emphasize the level of conviction, preoccupation, and extension of a belief rather than the content of the belief when considering whether a belief is delusional.It is important to distinguish true delusions from other symptoms such as anxiety, fear, or paranoia. To diagnose delusions a mental state examination may be used. This test includes appearance, mood, affect, behavior, rate and continuity of speech, evidence of hallucinations or abnormal beliefs, thought content, orientation to time, place and person, attention and concentration, insight and judgment, as well as short-term memory.Johnson-Laird suggests that delusions may be viewed as the natural consequence of failure to distinguish conceptual relevance. That is, irrelevant information would be framed as disconnected experiences, then it is taken to be relevant in a manner that suggests false causal connections. Furthermore, relevant information would be ignored as counterexamples.

Definition
Although non-specific concepts of madness have been around for several thousand years, the psychiatrist and philosopher Karl Jaspers was the first to define the four main criteria for a belief to be considered delusional in his 1913 book General Psychopathology. These criteria are:

certainty (held with absolute conviction)
incorrigibility (not changeable by compelling counterargument or proof to the contrary)
impossibility or falsity of content (implausible, bizarre, or patently untrue)
not amenable to understanding (i.e., belief cannot be explained psychologically)Furthermore, when beliefs involve value judgments, only those which cannot be proven true are considered delusions. For example: a man claiming that he flew into the Sun and flew back home. This would be considered a delusion, unless he were speaking figuratively, or if the belief had a cultural or religious source. Only the first three criteria remain cornerstornes of the current definition of a delusion in the DSM-5.
Robert Trivers writes that delusion is a discrepancy in relation to objective reality, but with a firm conviction in reality of delusional ideas, which is manifested in the "affective basis of delusion."

Treatment
Delusions and other positive symptoms of psychosis are often treated with antipsychotic medication, which exert a medium effect size according to meta-analytic evidence. Cognitive behavioral therapy (CBT) improves delusions relative to control conditions according to a meta-analysis. A meta-analysis of 43 studies reported that metacognitive training (MCT) reduces delusions at a medium to large effect size relative to control conditions.

Criticism
Some psychiatrists criticize the practice of defining one and the same belief as normal in one culture and pathological in another culture for cultural essentialism </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 Hypersomnia and explain in detail? [/INST] Hypersomnia is a neurological disorder of excessive time spent sleeping or excessive sleepiness. It can have many possible causes (such as seasonal affective disorder) and can cause distress and problems with functioning. In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), hypersomnolence, of which there are several subtypes, appears under sleep-wake disorders.Hypersomnia is a pathological state characterized by a lack of alertness during the waking episodes of the day. It is not to be confused with fatigue, which is a normal physiological state. Daytime sleepiness appears most commonly during situations where little interaction is needed.Since the patients’ attention levels (wakefulness) are impaired, their quality of life may be impacted as well. This is especially true for people whose jobs request high levels of attention, such as in the healthcare field.

Symptoms
The main symptom of hypersomnia is excessive daytime sleepiness (EDS), or prolonged nighttime sleep, which has occurred for at least 3 months prior to diagnosis.Sleep drunkenness is also a symptom found in hypersomniac patients. It is a difficulty transitioning from sleep to wake. Individuals experiencing sleep drunkenness report waking with confusion, disorientation, slowness and repeated returns to sleep.It also appears in non-hypersomniac persons, for example after a night of insufficient sleep. Fatigue and consumption of alcohol or hypnotics can cause sleep drunkenness as well. It is also associated with irritability: people who get angry shortly before sleeping tend to experience sleep drunkenness.According to the American Academy of Sleep Medicine, hypersomniac patients often take long naps during the day that are mostly unrefreshing. Researchers found that naps are usually more frequent and longer in patients than in controls. Furthermore, 75% of the patients report that short naps are not refreshing, compared to controls.

Diagnosis
"The severity of daytime sleepiness needs to be quantified by subjective scales (at least the Epworth Sleepiness Scale) and objective tests such as the multiple sleep latency test (MSLT)." The Stanford sleepiness scale (SSS) is another frequently-used subjective measurement of sleepiness. After it is determined that excessive daytime sleepiness is present, a complete medical examination and full evaluation of potential disorders in the differential diagnosis (which can be tedious, expensive and time-consuming) should be undertaken.

Differential diagnosis
Hypersomnia can be primary (of central/brain origin), or it can be secondary to any of numerous medical conditions. More than one type of hypersomnia can coexist in a single patient. Even in the presence of a known cause of hypersomnia, the contribution of this cause to the complaint of excessive daytime sleepiness needs to be assessed. When specific treatments of the known condition do not fully suppress excessive daytime sleepiness, additional causes of hypersomnia should be sought. For example, if a patient with sleep apnea is treated with CPAP (continuous positive airway pressure), which resolves their apneas but not their excessive daytime sleepiness, it is necessary to seek other causes for the excessive daytime sleepiness. Obstructive sleep apnea "occurs frequently in narcolepsy and may delay the diagnosis of narcolepsy by several years and interfere with its proper management."

Primary hypersomnias
The true primary hypersomnias include:
Narcolepsy (with and without cataplexy)
Idiopathic hypersomnia
Recurrent hypersomnias (like Kleine-Levin syndrome)

Primary hypersomnia mimics
There are also several genetic disorders that may be associated with primary/central hypersomnia. These include the following: Prader-Willi syndrome; Norrie disease; Niemann–Pick disease, type C; and myotonic dystrophy.  However, hypersomnia in these syndromes may also be associated with other secondary causes, so it is important to complete a full evaluation. Myotonic dystrophy is often associated with SOREMPs (sleep onset REM periods, such as occur in narcolepsy).There are many neurological disorders that may mimic the primary hypersomnias, narcolepsy and idiopathic hypersomnia: brain tumors; stroke-provoking lesions; and dysfunction in the thalamus, hypothalamus, or brainstem.  Also, neurodegenerative conditions such as Alzheimers disease, Parkinsons disease, or multiple system atrophy are frequently associated with primary hypersomnia. However, in these cases, one must still rule out other secondary causes.Early hydrocephalus can also cause severe excessive daytime sleepiness. Additionally, head trauma can be associated with a primary/central hypersomnia, and symptoms similar to those of idiopathic hypersomnia can be seen within 6–18 months following the trauma. However, the associated symptoms of headaches, memory loss, and lack of concentration may be more frequent in head trauma than in idiopathic hypersomnia. "The possibility of secondary narcolepsy following head injury in previously asymptomatic individuals has also been reported."

Secondary hypersomnias
Secondary hypersomnias are extremely numerous.
Hypersomnia can be secondary to disorders such as clinical depression, multiple sclerosis, encephalitis, epilepsy, or obesity. Hypersomnia can also be a symptom of other sleep disorders, like sleep apnea. It may occur as an adverse effect of taking certain medications, of withdrawal from some medications, or of substance use. A genetic predisposition may also be a factor. In some cases it results from a physical problem, such as a tumor, head trauma, or dysfunction of the autonomic or central nervous system.Sleep apnea is the second most frequent cause of secondary hypersomnia, affecting up to 4% of middle-aged adults, mostly men. Upper airway resistance syndrome (UARS) is a clinical variant of sleep apnea that can also cause hypersomnia. Just as other sleep disorders (like narcolepsy) can coexist with sleep apnea, the same is true for UARS. There are many cases of UARS in which excessive daytime sleepiness persists after CPAP treatment, indicating an additional cause, or causes, of the hypersomnia and requiring further evaluation.Sleep movement disorders, such as restless legs syndrome (RLS) and periodic limb movement disorder (PLMD or PLMS) can also cause secondary hypersomnia. Although RLS does commonly cause excessive daytime sleepiness, PLMS does not. There is no evidence that PLMS plays "a role in the etiology of daytime sleepiness. In fact, two studies showed no correlation between PLMS and objective measures of excessive daytime sleepiness. In addition, EDS in these patients is best treated with psychostimulants—and not with dopaminergic agents known to suppress PLMS."Neuromuscular diseases and spinal cord diseases often lead to sleep disturbances due to respiratory dysfunction causing sleep apnea, and they may also cause insomnia related to pain. "Other sleep alterations, such as periodic limb movement disorders in patients with spinal cord disease, have also been uncovered with the widespread use of polysomnography."Primary hypersomnia in diabetes, hepatic encephalopathy, and acromegaly is rarely reported, but these medical conditions may also be associated with hypersomnia secondary to sleep apnea and periodic limb movement disorder (PLMD).Chronic fatigue syndrome and fibromyalgia can also be associated with hypersomnia. Chronic fatigue syndrome is "characterized by persistent or relapsing fatigue that does not resolve with sleep or rest. Polysomnography shows reduced sleep efficiency and may include alpha intrusion into sleep EEG. It is likely that a number of cases labeled as chronic fatigue syndrome are unrecognized cases of upper airway resistance syndrome" or other sleep disorders, such as narcolepsy, sleep apnea, PLMD, etc.As with chronic fatigue syndrome, fibromyalgia may be associated with anomalous alpha wave activity (typically associated with arousal states) during NREM sleep. Also, researchers have shown that disrupting stage IV sleep consistently in young, healthy subjects causes a significant increase in muscle tenderness—similar to that experienced in "neurasthenic musculoskeletal pain syndrome". This pain resolved when the subjects were able to resume their normal sleep patterns.Chronic kidney disease is commonly associated with sleep symptoms and excessive daytime sleepiness. 80% of those on dialysis have sleep disturbances. Sleep apnea can occur 10 times as often in uremic patients than in the general population and can affect up to 30-80% of patients on dialysis, though nighttime dialysis can improve this. About 50% of dialysis patients have hypersomnia, as severe kidney disease can cause uremic encephalopathy, increased sleep-inducing cytokines, and impaired sleep efficiency. About 70% of dialysis patients are affected by insomnia, and RLS and PLMD affect 30%, though these may improve after dialysis or kidney transplant.Most forms of cancer and their therapies can cause fatigue and disturbed sleep, affecting 25-99% of patients and often lasting for years after treatment completion. "Insomnia is common and a predictor of fatigue in cancer patients, and polysomnography demonstrates reduced sleep efficiency, prolonged initial sleep latency, and increased wake time during the night." Paraneoplastic syndromes can also cause insomnia, hypersomnia, and parasomnias.Autoimmune diseases, especially lupus and rheumatoid arthritis, are often associated with hypersomnia. Morvans syndrome is an example of a rarer autoimmune illness that can also lead to hypersomnia. Celiac disease is another autoimmune disease associated with poor sleep quality (which may lead to hypersomnia), "not only at diagnosis but also during treatment with a gluten-free diet." There are also some case reports of central hypersomnia in celiac disease. And RLS "has been shown to be frequent in celiac disease," presumably due to its associated iron deficiency.Hypothyroidism and iron deficiency with or without (iron-deficiency anemia) can also cause secondary hypersomnia. Various tests for these disorders are done so they can be treated. Hypersomnia can also develop within months after viral infections such as Whipples disease, mononucleosis, HIV, and Guillain–Barré syndrome.Behaviorally induced insufficient sleep syndrome must be considered in the differential diagnosis of secondary hypersomnia. This disorder occurs in individuals who fail to get sufficient sleep for at least three months. In this case, the patient has chronic sleep deprivation, although they may not necessarily be aware of it. This situation is becoming more prevalent in western society due to the modern demands and expectations placed upon the individual.Many medications can lead to secondary hypersomnia. Therefore, a patients complete medication list should be carefully reviewed for sleepiness or fatigue as side effects. In these cases, careful withdrawal from the possibly offending medication(s) is needed; then, medication substitution can be undertaken.Mood disorders, like depression, anxiety disorder and bipolar disorder, can also be associated with hypersomnia. The complaint of excessive daytime sleepiness in these conditions is often associated with poor sleep at night. "In that sense, insomnia and EDS are frequently associated, especially in cases of depression." Hypersomnia in mood disorders seems to be primarily related to "lack of interest and decreased energy inherent in the depressed condition rather than an increase in sleep or REM sleep propensity". In all cases with these mood disorders, the MSLT is normal (not too short and no SOREMPs).

Posttraumatic hypersomnias
In some cases, hypersomnia can be caused by a brain injury. Researchers found that the level of sleepiness is correlated with the severity of the injury. Even if patients reported an improvement, sleepiness remained present for a year in about a quarter of patients with traumatic brain injury.

Recurrent hypersomnias
Recurrent hypersomnias are defined by several episodes of hypersomnia persisting from a few days to weeks. These episodes can occur weeks or months apart from each other. There are 2 subtypes of recurrent hypersomnias: Kleine-Levin syndrome and menstrual-related hypersomnia.Kleine-Levin syndrome is characterized by the association of episodes of hypersomnias with behavioral, cognitive and mood abnormalities. The behavioral disturbances can be composed of hyperphagia, irritability, or sexual disinhibition. The cognitive disorders consist of confusion, hallucinations or delusions. Mood symptoms are characterized by anxiety or depression.Menstrual-related hypersomnia is characterized by episodes of excessive sleepiness associated with the menstrual cycle. Researchers found that the degree of premenstrual symptoms were correlated with daytime sleepiness. Unlike Kleine-Levin syndrome, hyperphagia and hypersexuality are not reported in people with menstrual-related hypersomnia, but hypophagia could be present. Ordinarily, these episodes appear 2 weeks before menstruation. A few studies have attested that some hormones as prolactin and progesterone could be responsible for Menstrual-Related Hypersomnia. Therefore, different contraceptive pills could improve the symptoms. The sleep architecture changes. There is a decrease of slow-wave sleep and an increase of slow-Theta-wave activity.

Assessment tools
Polysomnography
Polysomnography is an objective sleep assessment method. It comprises a lot of electrodes which measure physiological variables related to sleep. Polysomnography often includes electroencephalography, electromyography, electrocardiography, muscle activity and respiratory function.Polysomnography is helpful to identify the very short sleep onset latency period, the very efficient sleep (more than 90%), the increased slow wave sleep, and sometimes an elevated amount of sleep spindles in idiopathic hypersomnia patients.

Multiple sleep latency test (MSLT)
The multiple sleep latency test (MSLT) is an objective tool which indicates the degree of sleepiness by measuring the sleep latency (i.e. the speed of falling asleep). It also gives information regarding the presence of abnormal REM sleep onset episodes. During that test, patients have a series of opportunities to sleep at 2-h intervals across the day in a darkened room and with no external alerting influences.The MSLT is often administered the day after recording the polysomnography, and the mean sleep latency score is often found to be around (or less than) 8 minutes in idiopathic hypersomnia patients. Some patients might even have a sleep onset latency of 5 minutes or less. These patients are often even more aware of sleeping during naps than narcolepsy patients.

Actigraphy
Actigraphy, which operates by analyzing the patients limb movements, is used to record the sleep and wake cycles. In order to report them, the patient has to wear continuously a device on his or her wrist, which looks like a watch and does not contain any electrodes.
The advantage actigraphy shows over polysomnography is that it is possible to record for 24-hours a day for weeks. Furthermore, unlike the polysomnography, it is less expensive and non-invasive.An actigraphy over several days can show longer sleep periods, which are characteristic for idiopathic hypersomnia. Actigraphy is also helpful in ruling out other sleep disorders, especially circadian disorders, leading to an excess of sleepiness during the day, too.

The maintenance of wakefulness test (MWT)
The maintenance of wakefulness test (MWT) is a test that measures the ability to stay awake. It is used to diagnose disorders of excessive somnolence, such as hypersomnia, narcolepsy or obstructive sleep apnea. During that test, patients sit comfortably and are instructed to try to stay awake.

The Stanford sleepiness scale (SSS)
The Stanford sleepiness scale (SSS) is a self-report scale that measures the different steps of sleepiness. For each statement, patients report their level of sleepiness using a 7-point scale, going from very alert to excessively sleepy </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 Pectus carinatum and explain in detail? [/INST] Pectus carinatum, also called pigeon chest, is a malformation of the chest characterized by a protrusion of the sternum and ribs. It is distinct from the related malformation pectus excavatum.

Signs and symptoms
People with pectus carinatum usually develop normal hearts and lungs, but the malformation may prevent these from functioning optimally. In moderate to severe cases of pectus carinatum, the chest wall is rigidly held in an outward position. Thus, respirations are inefficient and the individual needs to use the accessory muscles for respiration, rather than normal chest muscles, during strenuous exercise. This negatively affects gas exchange and causes a decrease in stamina. Children with pectus malformations often tire sooner than their peers due to shortness of breath and fatigue. Commonly concurrent is mild to moderate asthma.
Some children with pectus carinatum also have scoliosis (i.e., curvature of the spine). Some have mitral valve prolapse, a condition in which the heart mitral valve functions abnormally. Connective tissue disorders involving structural abnormalities of the major blood vessels and heart valves are also seen. Although rarely seen, some children have other connective tissue disorders, including arthritis, visual impairment and healing impairment.
Apart from the possible physiologic consequences, pectus malformations can have a significant psychologic impact. Some people, especially those with milder cases, live happily with pectus carinatum. For others, though, the shape of the chest can damage their self-image and confidence, possibly disrupting social connections and causing them to feel uncomfortable throughout adolescence and adulthood. As the child grows older, bodybuilding techniques may be useful for balancing visual impact.A less common variant of pectus carinatum is pectus arcuatum (also called type 2 pectus excavatum, chondromanubrial malformation or Currarino–Silverman syndrome or pouter pigeon malformation), which produces a manubrial and upper sternal protrusion, particularly also at the sternal angle. Pectus arcuatum is often confused with a combination of pectus carinatum and pectus excavatum, but in pectus arcuatum the visual appearance is characterized by a protrusion of the costal cartilages and there is no depression of the sternum.

Causes
Pectus carinatum is an overgrowth of costal cartilage causing the sternum to protrude forward. It primarily occurs among four different patient groups, and males are more frequently affected than females.  Most commonly, pectus carinatum develops in 11-to-14-year-old pubertal males undergoing a growth spurt. Some parents report that their childs pectus carinatum seemingly popped up overnight. Second most common is the presence of pectus carinatum at or shortly after birth. The condition may be evident in newborns as a rounded anterior chest wall. As the child reaches age 2 or 3 years of age, the outward sternal protrusion becomes more pronounced. Pectus carinatum can also be caused by vitamin D deficiency in children (Rickets) due to deposition of unmineralized osteoid. Least common is a pectus carinatum malformation following open-heart surgery or in children with poorly controlled bronchial asthma.
Pectus carinatum is generally a solitary, non-syndromic abnormality. However, the condition may be present in association with other syndromes: Turner syndrome, Noonan syndrome, Loeys–Dietz syndrome, Marfan syndrome, Ehlers–Danlos syndrome, Morquio syndrome, trisomy 18, trisomy 21, homocystinuria, osteogenesis imperfecta, multiple lentigines syndrome (LEOPARD syndrome), Sly syndrome (mucopolysaccharidosis type VII), and scoliosis.
In about 25% of cases of pectus carinatum, the patient has a family member with the condition.

Diagnosis
The pectus carinatum can be easily diagnosed by certain tests like a CT scan (2D and 3D). It may then be found out that the rib cage is in normal structure. If there is more than average growth of sternum than pectus carinatum protrudes. Also it is of two types, as pectus carinatum is symmetrical or unsymmetrical. On the basis of that further treatment is given to the patient.

Treatment
External bracing technique
The use of orthotic bracing, pioneered by Sydney Haje as of 1977, is finding increasing acceptance as an alternative to surgery in select cases of pectus carinatum. In children, teenagers, and young adults who have pectus carinatum and are motivated to avoid surgery, the use of a customized chest-wall brace that applies direct pressure on the protruding area of the chest produces excellent outcomes. Willingness to wear the brace as required is essential for the success of this treatment approach. The brace works in much the same way as orthodontics (braces that correct the alignment of teeth). The brace consists of front and back compression plates that are anchored to aluminum bars. These bars are bound together by a tightening mechanism which varies from brace to brace. This device is easily hidden under clothing and must be worn from 14 to 24 hours a day. The wearing time varies with each brace manufacturer and the managing physicians protocol, which could be based on the severity of the carinatum malformation (mild moderate severe) and if it is symmetric or asymmetric.Depending on the manufacturer and/or the patients preference, the brace may be worn on the skin or it may be worn over a body sock or sleeve called a Bracemate, specifically designed to be worn under braces. A physician or orthotist or brace manufacturers representative can show how to check to see if the brace is in correct position on the chest.Bracing is becoming more popular over surgery for pectus carinatum, mostly because it eliminates the risks that accompany surgery. The prescribing of bracing as a treatment for pectus carinatum has trickled down from both paediatric and thoracic surgeons to the family physician and pediatricians again due to its lower risks and well-documented very high success results. The pectus carinatum guideline of 2012 of the American Pediatric Surgical Association has stated: "As reconstructive therapy for the compliant pectus [carinatum] malformation, nonoperative compressive orthotic bracing is usually an appropriate first line of therapy as it does not preclude the operative option. For appropriate candidates, orthotic bracing of chest wall malformations can reasonably be expected to prevent worsening of the malformation and often results in a lasting correction of the malformation. Orthotic bracing is often successful in prepubertal children whose chest wall is compliant. Expert opinion suggests that the noncompliant chest wall malformation or significant asymmetry of the pectus carinatum malformation caused by a concomitant excavatum-type malformation may not respond to orthotic bracing."Regular supervision during the bracing period is required for optimal results. Adjustments may be needed to the brace as the child grows and the pectus improves.

Surgical
For patients with severe pectus carinatum, surgery may be necessary. However bracing could and may still be the first line of treatment </s>