<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Mania and can you explain it in depth? [/INST] Mania, also known as manic syndrome, is a mental and behavioral disorder defined as a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or dysphoric. As the mania intensifies, irritability can be more pronounced and result in anxiety or anger.
The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Causes and diagnosis
Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania (delirium), or stage III. This "staging" of a manic episode is useful from a descriptive and differential diagnostic point of view Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification
Mixed states
In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting "true" polar opposites, are, rather, two independent axes in a unipolar—bipolar spectrum.
A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Hypomania
Hypomania, which means "less than mania", is a lowered state of mania that does little to impair function or decrease quality of life. Although creativity and hypomania have been historically linked, a review and meta-analysis exploring this relationship found that this assumption may be too general and empirical research evidence is lacking. In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, some failed to detect differences. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, true mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable as opposed to euphoric, be a rather unpleasant experience. In addition, the exaggerated case of hypomania can lead to problems. For instance, trait-based positivity for a person could make them more engaging and outgoing, and cause them to have a positive outlook in life. When exaggerated in hypomania, however, such a person can display excessive optimism, grandiosity, and poor decision making, often with little regard to the consequences.

Associated disorders
A single manic episode, in the absence of secondary causes, (i.e., substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix "-mania," namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders.
Furthermore, evidence indicates a B12 deficiency can also cause symptoms characteristic of mania and psychosis.Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and symptoms
A manic episode is defined in the American Psychiatric Associations diagnostic manual as a "distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalization is necessary)," where the mood is not caused by drugs/medication or a non-mental medical illness (e.g., hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person has psychosis.To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

Inflated self-esteem or grandiosity.
Decreased need for sleep (e.g., feels rested after 3 hours of sleep).
More talkative than usual, or acts pressured to keep talking.
Flights of ideas or subjective experience that thoughts are racing.
Increase in goal-directed activity, or psychomotor acceleration.
Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
Excessive involvement in activities with a high likelihood of painful consequences.(e.g., extravagant shopping, improbable commercial schemes, hypersexuality).Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.
If the person is concurrently depressed, they are said to be having a mixed episode.The World Health Organizations classification system defines a manic episode as one where mood is higher than the persons situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behavior that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic persons connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those with prolonged unresolved hypomania do run the risk of developing full mania, and may cross that "line" without even realizing they have done so.One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individuals thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.
Manic states are always relative to the normal state of intensity of the affected individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly "genius" characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or "over-happy". Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally "wide open", rarely blinking, and may contribute to some clinicians erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behavior during the episode, such as questionable business transactions, wasteful expenditures of money (e.g., spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behavior (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.Although "severely elevated mood" sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the individuals lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.
Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bells), respectively.

Causes
Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69 percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.Deep brain stimulation of the subthalamic nucleus in Parkinsons disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.There are certain psychoactive drugs that can induce a state of manic psychosis, including: amphetamine, cathinone, cocaine, MDMA, methamphetamine, methylphenidate, oxycodone, phencyclidine, designer drugs, etc.Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism
The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioral changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-estrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests
a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.Limited evidence suggests that mania is associated with behavioral reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioral activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis
In the ICD-10 there are several disorders with the manic syndrome: organic manic disorder (F06.30), mania without psychotic symptoms (F30.1), mania with psychotic symptoms (F30.2), other manic episodes (F30.8), unspecified manic episode (F30.9), manic type of schizoaffective disorder (F25.0), bipolar disorder, current episode manic without psychotic symptoms (F31.1), bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).

Treatment
Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.
The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, aripiprazole, or cariprazine). The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patients mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.
In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.
Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and culture
In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as "the most perfect prescription glasses with which to see the world... life appears in front of you like an oversized movie screen".  Behrman indicates early in his memoir that he sees himself not as a person with an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries have bipolar disorder more often than those in other occupations.Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.English actor Stephen Fry, who has bipolar disorder, recounts manic behaviour during his adolescence: "When I was about 17 ... going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails." While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

Etymology
The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), "madness, frenzy" and the verb μαίνομαι (maínomai), "to be mad, to rage, to be furious".

See also
References
Further reading
Expert Opin Pharmacother. 2001 December;2(12):1963–73.
Schizoaffective Disorder. 2007 September Mayo Clinic. Retrieved October 1, 2007.
Schizoaffective Disorder Archived 2011-08-18 at the Wayback Machine. 2004 May </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sebaceous cyst and can you explain it in depth? [/INST] A sebaceous cyst is a term commonly used to refer to either:
Epidermoid cysts (also termed epidermal cysts, infundibular cyst)
Pilar cysts (also termed trichelemmal cysts, isthmus-catagen cysts)Both of the above types of cysts contain keratin, not sebum, and neither originates from sebaceous glands. Epidermoid cysts originate in the epidermis and pilar cysts originate from hair follicles. Technically speaking, then, they are not sebaceous cysts. "True" sebaceous cysts,  which originate from sebaceous glands and which contain sebum, are relatively rare and are known as steatocystoma simplex or, if multiple, as steatocystoma multiplex.
Medical professionals have suggested that the term "sebaceous cyst" be avoided since it can be misleading.: 31  In practice, however, the term is still often used for epidermoid and pilar cysts.

Signs and symptoms
The scalp, ears, back, face, and upper arm, are common sites of sebaceous cysts, though they may occur anywhere on the body except the palms of the hands and soles of the feet. They are more common in hairier areas, where in cases of long duration they could result in hair loss on the skin surface immediately above the cyst. They are smooth to the touch, vary in size, and are generally round in shape.
They are generally mobile masses that can consist of:

Fibrous tissues and fluids
A fatty (keratinous) substance that resembles cottage cheese, in which case the cyst may be called "keratin cyst" - this material has a characteristic "cheesy" or foot odor smell
A somewhat viscous, serosanguineous fluid (containing purulent and bloody material)The nature of the contents of a sebaceous cyst, and of its surrounding capsule, differs depending on whether the cyst has ever been infected.
With surgery, a cyst can usually be excised in its entirety. Poor surgical technique, or previous infection leading to scarring and tethering of the cyst to the surrounding tissue, may lead to rupture during excision and removal </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bulimia nervosa and can you explain it in depth? [/INST] Bulimia nervosa, also known as simply bulimia, is an eating disorder characterized by binge eating followed by purging or fasting, and excessive concern with body shape and weight. The aim of this activity is to expel the body of calories eaten from the binging phase of the process. Binge eating refers to eating a large amount of food in a short amount of time. Purging refers to the attempts to get rid of the food consumed. This may be done by vomiting or taking laxatives. Other efforts to lose weight may include the use of diuretics, stimulants, water fasting, or excessive exercise. Most people with bulimia are at a normal weight. The forcing of vomiting may result in thickened skin on the knuckles, breakdown of the teeth and effects on metabolic rate and caloric intake which cause thyroid dysfunction. Bulimia is frequently associated with other mental disorders such as depression, anxiety, borderline personality disorder, bipolar disorder and problems with drugs or alcohol. There is also a higher risk of suicide and self-harm.Bulimia is more common among those who have a close relative with the condition. The percentage risk that is estimated to be due to genetics is between 30% and 80%. Other risk factors for the disease include psychological stress, cultural pressure to attain a certain body type, poor self-esteem, and obesity. Living in a culture that commercializes or glamorizes dieting and having parental figures who fixate about weight are also risks. Diagnosis is based on a persons medical history; however, this is difficult, as people are usually secretive about their binge eating and purging habits. Further, the diagnosis of anorexia nervosa takes precedence over that of bulimia. Other similar disorders include binge eating disorder, Kleine–Levin syndrome, and borderline personality disorder.

Signs and symptoms
Bulimia typically involves rapid and out-of-control eating, which may stop when the person is interrupted by another person or the stomach hurts from over-extension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day and may directly cause:

Chronic gastric reflux after eating, secondary to vomiting
Dehydration and hypokalemia due to renal potassium loss in the presence of alkalosis and frequent vomiting
Electrolyte imbalance, which can lead to abnormal heart rhythms, cardiac arrest, and even death
Esophagitis, or inflammation of the esophagus
Mallory-Weiss tears
Boerhaave syndrome, a rupture in the esophageal wall due to vomiting
Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat
Russells sign: calluses on knuckles and back of hands due to repeated trauma from incisors
Perimolysis, or severe dental erosion of tooth enamel
Swollen salivary glands (for example, in the neck, under the jaw line)
Gastroparesis, or delayed gastric emptying
Constipation or diarrhea
Tachycardia or palpitations
Hypotension
Peptic ulcers
Infertility
Constant weight fluctuations are common
Elevated blood sugar, cholesterol, and amylase levels may occur
Hypoglycemia may occur after vomitingThese are some of the many signs that may indicate whether someone has bulimia nervosa:
A fixation on the number of calories consumed
A fixation on and extreme consciousness of ones weight
Low self-esteem and/or self-harming
Suicidal tendencies
An irregular menstrual cycle in women
Regular trips to the bathroom, especially soon after eating
Depression, anxiety disorders and sleep disorders
Frequent occurrences involving consumption of abnormally large portions of food
The use of laxatives, diuretics, and diet pills
Compulsive or excessive exercise
Unhealthy/dry skin, hair, nails, and lips
Fatigue, or exhaustionAs with many psychiatric illnesses, delusions can occur, in conjunction with other signs and symptoms, leaving the person with a false belief that is not ordinarily accepted by others.People with bulimia nervosa may also exercise to a point that excludes other activities.

Interoceptive
People with bulimia exhibit several interoceptive deficits, in which one experiences impairment in recognizing and discriminating between internal sensations, feelings, and emotions. People with bulimia may also react negatively to somatic and affective states. In relation to interoceptive sensitivity, hyposensitive individuals may not detect feelings of fullness in a normal and timely fashion, and therefore are prone to eating more calories.Examining from a neural basis also connects elements of interoception and emotion; notable overlaps occur in the medial prefrontal cortex, anterior and posterior cingulate, and anterior insula cortices, which are linked to both interoception and emotional eating.

Related disorders
People with bulimia are at a higher risk to have an affective disorder, such as depression or general anxiety disorder. One study found 70% had depression at some time in their lives (as opposed to 26% for adult females in the general population), rising to 88% for all affective disorders combined. Another study in the Journal of Affective Disorders found that of the population of patients that were diagnosed with an eating disorder according to the DSM-V guidelines about 27% also suffered from bipolar disorder. Within this article, the majority of the patients were diagnosed with  bulimia nervosa, the second most common condition reported was binge-eating disorder.Some individuals with anorexia nervosa exhibit episodes of bulimic tendencies through purging (either through self-induced vomiting or laxatives) as a way to quickly remove food in their system. There may be an increased risk for diabetes mellitus type 2. Bulimia also has negative effects on a persons teeth due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.
Research has shown that there is a relationship between bulimia and narcissism. According to a study by the Australian National University, eating disorders are more susceptible among vulnerable narcissists. This can be caused by a childhood in which inner feelings and thoughts were minimized by parents, leading to "a high focus on receiving validation from others to maintain a positive sense of self".The medical journal Borderline Personality Disorder and Emotion Dysregulation notes that a "substantial rate of patients with bulimia nervosa" also have Borderline personality disorder.A study by the Psychopharmacology Research Program of the University of Cincinnati College of Medicine "leaves little doubt that bipolar and eating disorders—particularly bulimia nervosa and bipolar II disorder—are related." The research shows that most clinical studies indicate that patients with bipolar disorder have higher rates of eating disorders, and vice versa. There is overlap in phenomenology, course, comorbidity, family history, and pharmacologic treatment response of these disorders. This is especially true of "eating dysregulation, mood dysregulation, impulsivity and compulsivity, craving for activity and/or exercise."Studies have shown a relationship between bulimias effect on metabolic rate and caloric intake with thyroid dysfunction.

Causes
Biological
As with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder. Abnormal levels of many hormones, notably serotonin, have been shown to be responsible for some disordered eating behaviors. Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.There is evidence that sex hormones may influence appetite and eating in women and the onset of bulimia nervosa. Studies have shown that women with hyperandrogenism and polycystic ovary syndrome have a dysregulation of appetite, along with carbohydrates and fats. This dysregulation of appetite is also seen in women with bulimia nervosa. In addition, gene knockout studies in mice have shown that mice that have the gene encoding estrogen receptors have decreased fertility due to ovarian dysfunction and dysregulation of androgen receptors.  In humans, there is evidence that there is an association between polymorphisms in the ERβ (estrogen receptor β) and bulimia, suggesting there is a correlation between sex hormones and bulimia nervosa.Bulimia has been compared to drug addiction, though the empirical support for this characterization is limited. However, people with bulimia nervosa may share dopamine D2 receptor-related vulnerabilities with those with substance use disorders.Dieting, a common behaviour in bulimics, is associated with lower plasma tryptophan levels. Decreased tryptophan levels in the brain, and thus the synthesis of serotonin, such as via acute tryptophan depletion, increases bulimic urges in currently and formerly bulimic individuals within hours.Abnormal blood levels of peptides important for the regulation of appetite and energy balance are observed in individuals with bulimia nervosa, but it remains unknown if this is a state or trait.In recent years, evolutionary psychiatry as an emerging scientific discipline has been studying mental disorders from an evolutionary perspective. If eating disorders, Bulimia nervosa in particular, have evolutionary functions or if they are new modern "lifestyle" problems is still debated.

Social
Media portrayals of an ideal body shape are widely considered to be a contributing factor to bulimia. In a 1991 study by Weltzin, Hsu, Pollicle, and Kaye, it was stated that 19% of bulimics undereat, 37% of bulimics eat an average or normal amount of food, and 44% of bulimics overeat. A survey of 15- to 18-year-old high school girls in Nadroga, Fiji, found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998. In addition, the suicide rate among people with bulimia nervosa is 7.5 times higher than in the general population.When attempting to decipher the origin of bulimia nervosa in a cognitive context, Christopher Fairburn et al.s cognitive-behavioral model is often considered the golden standard. Fairburn et al.s model discusses the process in which an individual falls into the binge-purge cycle and thus develops bulimia. Fairburn et al. argue that extreme concern with weight and shape coupled with low self-esteem will result in strict, rigid, and inflexible dietary rules. Accordingly, this would lead to unrealistically restricted eating, which may consequently induce an eventual "slip" where the individual commits a minor infraction of the strict and inflexible dietary rules. Moreover, the cognitive distortion due to dichotomous thinking leads the individual to binge. The binge subsequently should trigger a perceived loss of control, promoting the individual to purge in hope of counteracting the binge. However, Fairburn et al. assert the cycle repeats itself, and thus consider the binge-purge cycle to be self-perpetuating.In contrast, Byrne and Mcleans findings differed slightly from Fairburn et al.s cognitive-behavioral model of bulimia nervosa in that the drive for thinness was the major cause of purging as a way of controlling weight. In turn, Byrne and Mclean argued that this makes the individual vulnerable to binging, indicating that it is not a binge-purge cycle but rather a purge-binge cycle in that purging comes before bingeing. Similarly, Fairburn et al.s cognitive-behavioral model of bulimia nervosa is not necessarily applicable to every individual and is certainly reductionist. Every one differs from another, and taking such a complex behavior like bulimia and applying the same one theory to everyone would certainly be invalid. In addition, the cognitive-behavioral model of bulimia nervosa is very culturally bound in that it may not be necessarily applicable to cultures outside of Western society. To evaluate, Fairburn et al..s model and more generally the cognitive explanation of bulimia nervosa is more descriptive than explanatory, as it does not necessarily explain how bulimia arises. Furthermore, it is difficult to ascertain cause and effect, because it may be that distorted eating leads to distorted cognition rather than vice versa.A considerable amount of literature has identified a correlation between sexual abuse and the development of bulimia nervosa. The reported incident rate of unwanted sexual contact is higher among those with bulimia nervosa than anorexia nervosa.When exploring the etiology of bulimia through a socio-cultural perspective, the "thin ideal internalization" is significantly responsible. The thin-ideal internalization is the extent to which individuals adapt to the societal ideals of attractiveness. Studies have shown that young women  that read fashion magazines tend to have more bulimic symptoms than those women who do not. This further demonstrates the impact of media on the likelihood of developing the disorder. Individuals first accept and "buy into" the ideals, and then attempt to transform themselves in order to reflect the societal ideals of attractiveness. J. Kevin Thompson and Eric Stice claim that family, peers, and most evidently media reinforce the thin ideal, which may lead to an individual accepting and "buying into" the thin ideal. In turn, Thompson and Stice assert that if the thin ideal is accepted, one could begin to feel uncomfortable with their body shape or size since it may not necessarily reflect the thin ideal set out by society. Thus, people feeling uncomfortable with their bodies may result in body dissatisfaction and may develop a certain drive for thinness. Consequently, body dissatisfaction coupled with a drive for thinness is thought to promote dieting and negative effects, which could eventually lead to bulimic symptoms such as purging or bingeing. Binges lead to self-disgust which causes purging to prevent weight gain.A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompsons and Stices research. Their study aimed to investigate how and to what degree media affects the thin ideal internalization. Thompson and Stice used randomized experiments (more specifically programs) dedicated to teaching young women how to be more critical when it comes to media, to reduce thin-ideal internalization. The results showed that by creating more awareness of the medias control of the societal ideal of attractiveness, the thin ideal internalization significantly dropped. In other words, less thin ideal images portrayed by the media resulted in less thin-ideal internalization. Therefore, Thompson and Stice concluded that media greatly affected the thin ideal internalization. Papies showed that it is not the thin ideal itself, but rather the self-association with other persons of a certain weight that decide how someone with bulimia nervosa feels. People that associate themselves with thin models get in a positive attitude when they see thin models and people that associate with overweight get in a negative attitude when they see thin models. Moreover, it can be taught to associate with thinner people.

Diagnosis
The onset of bulimia nervosa is often during adolescence, between 13 and 20 years of age, and many cases have previously experienced obesity, with many relapsing in adulthood into episodic bingeing and purging even after initially successful treatment and remission. A lifetime prevalence of 0.5 percent and 0.9 percent for adults and adolescents, respectively, is estimated among the United States population. Bulimia nervosa may affect up to 1% of young women and, after 10 years of diagnosis, half will recover fully, a third will recover partially, and 10–20% will still have symptoms.Adolescents with bulimia nervosa are more likely to have self-imposed perfectionism and compulsivity issues in eating compared to their peers. This means that the high expectations and unrealistic goals that these individuals set for themselves are internally motivated rather than by social views or expectations.

Criteria
Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above average weight. Many bulimics may also engage in significantly disordered eating and exercise patterns without meeting the full diagnostic criteria for bulimia nervosa. Recently, the Diagnostic and Statistical Manual of Mental Disorders was revised, which resulted in the loosening of criteria regarding the diagnoses of bulimia nervosa and anorexia nervosa. The diagnostic criteria utilized by the DSM-5 includes repetitive episodes of binge eating (a discrete episode of overeating during which the individual feels out of control of consumption) compensated for by excessive or inappropriate measures taken to avoid gaining weight. The diagnosis also requires the episodes of compensatory behaviors and binge eating to happen a minimum of once a week for a consistent time period of 3 months. The diagnosis is made only when the behavior is not a part of the symptom complex of anorexia nervosa and when the behavior reflects an overemphasis on physical mass or appearance. Purging often is a common characteristic of a more severe case of bulimia nervosa.

Treatment
There are two main types of treatment given to those with bulimia nervosa; psychopharmacological and psychosocial treatments.

Psychotherapy
Cognitive behavioral therapy is the primary treatment for bulimia. Antidepressants of the selective serotonin reuptake inhibitor (SSRI) or tricyclic antidepressant classes may have a modest benefit. While outcomes with bulimia are typically better than in those with anorexia, the risk of death among those affected is higher than that of the general population. At 10 years after receiving treatment about 50% of people are fully recovered.Cognitive behavioral therapy (CBT), which involves teaching a person to challenge automatic thoughts and engage in behavioral experiments (for example, in session eating of "forbidden foods") has a small amount of evidence supporting its use.By using CBT people record how much food they eat and periods of vomiting with the purpose of identifying and avoiding emotional fluctuations that bring on episodes of bulimia on a regular basis. Barker (2003) states that research has found 40–60% of people using cognitive behaviour therapy to become symptom free. He states in order for the therapy to work, all parties must work together to discuss, record and develop coping strategies. Barker (2003) claims by making people aware of their actions they will think of alternatives. People undergoing CBT who exhibit early behavioral changes are most likely to achieve the best treatment outcomes in the long run. Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.Maudsley family therapy, developed at the Maudsley Hospital in London for the treatment of anorexia, has been shown promising results in bulimia.The use of CBT has been shown to be quite effective for treating bulimia nervosa (BN) in adults, but little research has been done on effective treatments of BN for adolescents. Although CBT is seen as more cost-efficient and helps individuals with BN in self-guided care, Family Based Treatment (FBT) might be more helpful to younger adolescents who need more support and guidance from their families. Adolescents are at the stage where their brains are still quite malleable and developing gradually. Therefore, young adolescents with BN are less likely to realize the detrimental consequences of becoming bulimic and have less motivation to change, which is why FBT would be useful to have families intervene and support the teens. Working with BN patients and their families in FBT can empower the families by having them involved in their adolescents food choices and behaviors, taking more control of the situation in the beginning and gradually letting the adolescent become more autonomous when they have learned healthier eating habits.

Medication
Participating in some sort of therapy can be the best medication for bulimia. Antidepressants of the selective serotonin reuptake inhibitors (SSRI) class may have a modest benefit. This includes fluoxetine, also known as prozac, which is FDA approved, for the treatment of bulimia, other antidepressants such as sertraline may also be effective against bulimia. Topiramate may also be useful but has greater side effects. Compared to placebo, the use of a single antidepressant has been shown to be effective. Combining medication with counseling can improve outcomes in some circumstances. Some positive outcomes of treatments can include: abstinence from binge eating, a decrease in obsessive behaviors to lose weight and in shape preoccupation, less severe psychiatric symptoms, a desire to counter the effects of binge eating, as well as an improvement in social functioning and reduced relapse rates.

Alternative medicine
Some researchers have also claimed positive outcomes in hypnotherapy. The first use of hypnotherapy in Bulimic patients was in 1981. When it comes to hypnotherapy, Bulimic patients are easier to hypnotize than Anorexia Nervosa patients. In Bulimic patients, hypnotherapy focuses on learning self-control when it comes to binging and vomiting, strengthening stimulus control techniques, enhancing ones ego, improving weight control, and helping overweight patients see their body differently (have a different image).

Risk Factors
Being female and having bulimia nervosa takes a toll on mental health. Women frequently reported an onset of anxiety at the same time of the onset of bulimia nervosa. Another concern with eating disorders is developing a coexisting substance use disorder.

Epidemiology
There is little data on the percentage of people with bulimia in general populations. Most studies conducted thus far have been on convenience samples from hospital patients, high school or university students. These have yielded a wide range of results: between 0.1% and 1.4% of males, and between 0.3% and 9.4% of females. Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results. According to Gelder, Mayou and Geddes (2005) bulimia nervosa is prevalent between 1 and 2 percent of women aged 15–40 years. Bulimia nervosa occurs more frequently in developed countries and in cities, with one study finding that bulimia is five times more prevalent in cities than in rural areas. There is a perception that bulimia is most prevalent amongst girls from middle-class families; however, in a 2009 study girls from families in the lowest income bracket studied were 153 percent more likely to be bulimic than girls from the highest income bracket.There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance, gymnastics, modeling, cheerleading, running, acting, swimming, diving, rowing and figure skating. Bulimia is thought to be more prevalent among Caucasians; however, a more recent study showed that African-American teenage girls were 50 percent more likely than Caucasian girls to exhibit bulimic behavior, including both binging and purging.

History
Etymology
The term bulimia comes from Greek βουλιμία boulīmia, "ravenous hunger", a compound of βοῦς bous, "ox" and λιμός, līmos, "hunger". Literally, the scientific name of the disorder, bulimia nervosa, translates to "nervous ravenous hunger".

Before the 20th century
Although diagnostic criteria for bulimia nervosa did not appear until 1979, evidence suggests that binging and purging were popular in certain ancient cultures. The first documented account of behavior resembling bulimia nervosa was recorded in Xenophons Anabasis around 370 B.C, in which Greek soldiers purged themselves in the mountains of Asia Minor.  It is unclear whether this purging was preceded by binging. In ancient Egypt, physicians recommended purging once a month for three days to preserve health. This practice stemmed from the belief that human diseases were caused by the food itself. In ancient Rome, elite society members would vomit to "make room" in their stomachs for more food at all-day banquets. Emperors Claudius and Vitellius both were gluttonous and obese, and they often resorted to habitual purging.Historical records also suggest that some saints who developed anorexia (as a result of a life of asceticism) may also have displayed bulimic behaviors. Saint Mary Magdalen de Pazzi (1566–1607) and Saint Veronica Giuliani (1660–1727) were both observed binge eating—giving in, as they believed, to the temptations of the devil. Saint Catherine of Siena (1347–1380) is known to have supplemented her strict abstinence from food by purging as reparation for her sins. Catherine died from starvation at age thirty-three.While the psychological disorder "bulimia nervosa" is relatively new, the word "bulimia", signifying overeating, has been present for centuries. The Babylon Talmud referenced practices of "bulimia", yet scholars believe that this simply referred to overeating without the purging or the psychological implications bulimia nervosa. In fact, a search for evidence of bulimia nervosa from the 17th to late 19th century revealed that only a quarter of the overeating cases they examined actually vomited after the binges. There was no evidence of deliberate vomiting or an attempt to control weight.

20th century
Globally, bulimia was estimated to affect 3.6 million people in 2015. About 1% of young women have bulimia at a given point in time and about 2% to 3% of women have the condition at some point in their lives. The condition is less common in the developing world. Bulimia is about nine times more likely to occur in women than men. Among women, rates are highest in young adults. Bulimia was named and first described by the British psychiatrist Gerald Russell in 1979.At the turn of the century, bulimia (overeating) was described as a clinical symptom, but rarely in the context of weight control. Purging, however, was seen in anorexic patients and attributed to gastric pain rather than another method of weight control.In 1930, admissions of anorexia nervosa patients to the Mayo Clinic from 1917 to 1929 were compiled. Fifty-five to sixty-five percent of these patients were reported to be voluntarily vomiting to relieve weight anxiety. Records show that purging for weight control continued throughout the mid-1900s. Several case studies from this era reveal patients with the modern description of bulimia nervosa. In 1939, Rahman and Richardson reported that out of their six anorexic patients, one had periods of overeating, and another practiced self-induced vomiting. Wulff, in 1932, treated "Patient D", who would have periods of intense cravings for food and overeat for weeks, which often resulted in frequent vomiting. Patient D, who grew up with a tyrannical father, was repulsed by her weight and would fast for a few days, rapidly losing weight. Ellen West, a patient described by Ludwig Binswanger in 1958, was teased by friends for being fat and excessively took thyroid pills to lose weight, later using laxatives and vomiting. She reportedly consumed dozens of oranges and several pounds of tomatoes each day, yet would skip meals. After being admitted to a psychiatric facility for depression, Ellen ate ravenously yet lost weight, presumably due to self-induced vomiting </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pruritus vulvae and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Peristalsis and can you explain it in depth? [/INST] Peristalsis ( PERR-ih-STAL-siss, US also  -STAWL-) is a radially symmetrical contraction and relaxation of muscles that propagate in a wave down a tube, in an anterograde direction. Peristalsis is progression of coordinated contraction of involuntary circular muscles, which is preceded by a simultaneous contraction of the longitudinal muscle and relaxation of the circular muscle in the lining of the gut.In much of a digestive tract such as the human gastrointestinal tract, smooth muscle tissue contracts in sequence to produce a peristaltic wave, which propels a ball of food (called a bolus before being transformed into chyme in the stomach) along the tract. The peristaltic movement comprises relaxation of circular smooth muscles, then their contraction behind the chewed material to keep it from moving backward, then longitudinal contraction to push it forward.
Earthworms use a similar mechanism to drive their locomotion, and some modern machinery imitate this design.
The word comes from New Latin and is derived from the Greek peristellein, "to wrap around," from peri-, "around" + stellein, "draw in, bring together; set in order".

Human physiology
Peristalsis is generally directed caudal, that is, towards the anus. This sense of direction might be attributable to the polarisation of the myenteric plexus. Because of the reliance of the peristaltic reflex on the myenteric plexus, it is also referred to as the myenteric reflex.

Mechanism of the peristaltic reflex
The food bolus causes a stretch of the gut smooth muscle that causes serotonin to be secreted to sensory neurons, which then get activated. These sensory neurons, in turn, activate neurons of the myenteric plexus, which then proceed to split into two cholinergic pathways: a retrograde and an anterograde. Activated neurons of the retrograde pathway release substance P and acetylcholine to contract the smooth muscle behind the bolus. The activated neurons of the anterograde pathway instead release nitric oxide and vasoactive intestinal polypeptide to relax the smooth muscle caudal to the bolus. This allows the food bolus to effectively be pushed forward along the digestive tract.

Esophagus
After food is chewed into a bolus, it is swallowed and moved through the esophagus. Smooth muscles contract behind the bolus to prevent it from being squeezed back into the mouth. Then rhythmic, unidirectional waves of contractions work to rapidly force the food into the stomach. The migrating motor complex (MMC) helps trigger peristaltic waves. This process works in one direction only, and its sole esophageal function is to move food from the mouth into the stomach (the MMC also functions to clear out remaining food in the stomach to the small bowel and remaining particles in the small bowel into the colon).

In the esophagus, two types of peristalsis occur:

First, there is a primary peristaltic wave, which occurs when the bolus enters the esophagus during swallowing. The primary peristaltic wave forces the bolus down the esophagus and into the stomach in a wave lasting about 8–9 seconds. The wave travels down to the stomach even if the bolus of food descends at a greater rate than the wave itself, and continues even if for some reason the bolus gets stuck further up the esophagus.
If the bolus gets stuck or moves slower than the primary peristaltic wave (as can happen when it is poorly lubricated), then stretch receptors in the esophageal lining are stimulated and a local reflex response causes a secondary peristaltic wave around the bolus, forcing it further down the esophagus, and these secondary waves continue indefinitely until the bolus enters the stomach. The process of peristalsis is controlled by the medulla oblongata. Esophageal peristalsis is typically assessed by performing an esophageal motility study.
A third type of peristalsis, tertiary peristalsis, is dysfunctional and involves irregular, diffuse, simultaneous contractions. These contractions are suspect in esophageal dysmotility and present on a barium swallow as a "corkscrew esophagus".During vomiting, the propulsion of food up the esophagus and out the mouth comes from the contraction of the abdominal muscles; peristalsis does not reverse in the esophagus.

Stomach
When a peristaltic wave reaches at the end of the esophagus, the cardiac sphincter (gastroesophageal sphincter) opens, allowing the passage of bolus into the stomach. The gastroesophageal sphincter normally remains closed and does not allow the stomachs food contents to move back. The churning movements of the stomachs thick muscular wall blend the food thoroughly with the acidic gastric juice, producing a mixture called the chyme. The muscularis layer of the stomach is thickest and maximum peristalsis occurs here. After short intervals, the pyloric sphincter keeps on opening and closing so the chyme is fed into the intestine in installments.

Small intestine
Once processed and digested by the stomach, the semifluid chyme is passed through the pyloric sphincter into the small intestine. Once past the stomach, a typical peristaltic wave lasts only a few seconds, traveling at only a few centimeters per second. Its primary purpose is to mix the chyme in the intestine rather than to move it forward in the intestine. Through this process of mixing and continued digestion and absorption of nutrients, the chyme gradually works its way through the small intestine to the large intestine.In contrast to peristalsis, segmentation contractions result in that churning and mixing without pushing materials further down the digestive tract.

Large intestine
Although the large intestine has peristalsis of the type that the small intestine uses, it is not the primary propulsion. Instead, general contractions called mass action contractions occur one to three times per day in the large intestine, propelling the chyme (now feces) toward the rectum. Mass movements often tend to be triggered by meals, as the presence of chyme in the stomach and duodenum prompts them (gastrocolic reflex). Minimum peristalsis is found in the rectum part of the large intestine as a result of the thinnest muscularis layer.

Lymph
The human lymphatic system has no central pump. Instead, lymph circulates through peristalsis in the lymph capillaries as well as valves in the capillaries, compression during contraction of adjacent skeletal muscle, and arterial pulsation.

Sperm
During ejaculation, the smooth muscle in the walls of the vas deferens contracts reflexively in peristalsis, propelling sperm from the testicles to the urethra.

Earthworms
The earthworm is a limbless annelid worm with a hydrostatic skeleton that moves by peristalsis </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Le Fort fracture of skull and can you explain it in depth? [/INST] A Le Fort fracture of the skull is a classic transfacial fracture of the midface, involving the maxillary bone and surrounding structures in either a horizontal, pyramidal or transverse direction. The hallmark of Lefort fractures is traumatic pterygomaxillary separation, which signifies fractures between the pterygoid plates, horseshoe-shaped bony protuberances which extend from the inferior margin of the maxilla, and the maxillary sinuses. Continuity of this structure is a keystone for stability of the midface, involvement of which impacts surgical management of trauma victims, as it requires fixation to a horizontal bar of the frontal bone. The pterygoid plates lie posterior to the upper dental row, or alveolar ridge, when viewing the face from an anterior view. The fractures are named after French surgeon René Le Fort (1869–1951), who discovered the fracture patterns by examining crush injuries in cadavers.

Signs and symptoms
Le Fort I – Slight swelling of the upper lip, ecchymosis is present in the buccal sulcus beneath each zygomatic arch, malocclusion, mobility of teeth. Impacted type of fractures may be almost immobile and it is only by grasping the maxillary teeth and applying a little firm pressure that a characteristic grate can be felt which is diagnostic of the fracture. Percussion of upper teeth results in cracked pot sound. Guérins sign is present characterised by ecchymosis in the region of greater palatine vessels.Le Fort II and Le Fort III (common) – Gross edema of soft tissue over the middle third of the face, bilateral circumorbital ecchymosis, bilateral subconjunctival hemorrhage, epistaxis, CSF rhinorrhoea, dish face deformity, diplopia, enophthalmos, cracked pot sound.Le Fort II – Step deformity at infraorbital margin, mobile mid face, anesthesia or paresthesia of cheek.
Le Fort III – Tenderness and separation at frontozygomatic suture, lengthening of face, depression of ocular levels (enophthalmos), hooding of eyes, and tilting of occlusal plane, an imaginary curved plane between the edges of the incisors and the tips of the posterior teeth. As a result, there is gagging on the side of injury.

Diagnosis
Diagnosis is suspected by physical exam and history, in which, classically, the hard and soft palate of the midface are mobile with respect to the remainder of facial structures. This finding can be inconsistent due to the midfacial bleeding and swelling that typically accompany such injuries, and so confirmation is usually needed by radiograph or CT.

Classification
There are three types of Le Fort fractures. As the classification increases, the anatomic level of the maxillary fracture ascends from inferior to superior with respect to the maxilla:

Le Fort I fracture (horizontal), otherwise known as a floating palate, may result from a force of injury directed low on the maxillary alveolar rim, or upper dental row, in a downward direction. The essential component of these fractures, in addition to pterygoid plate involvement, is involvement of the lateral bony margin of the nasal opening. They also involve the medial and lateral buttresses, or walls, of the maxillary sinus, traveling through the face just above the alveolar ridge of the upper dental row. At the midline, the inferior nasal septum is involved. Historically, it has also been referred to as a Guérin fracture, although this name is less commonly used in practice.
Le Fort II fracture (pyramidal) may result from a blow to the lower or mid maxillary area. In addition to pterygoid plate disruption, their distinguishing component is involvement of inferior orbital rim. When viewed from the front, the fracture is classically shaped like a pyramid. It extends from the nasal bridge at or below the nasofrontal suture through the superior medial wall of the maxilla, inferolaterally through the lacrimal bones which contain the tear ducts, and inferior orbital floor through or near the infraorbital foramen.
Le Fort III fracture (transverse), otherwise known as craniofacial dissociation, may follow impact to the nasal bridge or upper maxilla. The salient feature of these fractures, beyond pterygoid plate involvement, is that they invariably involve the zygomatic arch, or cheek bone </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Classified and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Footedness and can you explain it in depth? [/INST] Footedness is the natural preference of ones left or right foot for various purposes. It is the foot equivalent of handedness. While purposes vary, such as applying the greatest force in a certain foot to complete the action of kick as opposed to stomping, footedness is most commonly associated with the preference of a particular foot in the leading position while engaging in foot- or kicking-related sports, such as association football and kickboxing. A person may thus be left-footed, right-footed or ambipedal (able to use both feet equally well).

Ball games
In association football, the ball is predominantly struck by the foot. Footedness may refer to the foot a player uses to kick with the greatest force and skill. Most people are right-footed, kicking with the right leg. Capable left-footed footballers are rare and therefore quite sought after. As rare are "two-footed" players, who are equally capable with both feet. Such players make up only one sixth of players in the top professional leagues in Europe. Two-footedness can be learnt, a notable case being England international Tom Finney, but can only be properly developed in the early years. In Australian Rules Football, several players are equally adept at using both feet to kick the ball, such as Sam Mitchell and Charles Bushnell (footballer, retired).In basketball, a sport composed almost solely of right-handed players, it is common for most athletes to have a dominant left leg which they would use when jumping to complete a right-hand layup. Hence, left-handed basketball players tend to use their right leg more as they finish a left handed layup (although both right- and left-handed players are usually able to use both hands when finishing near the basket).
In the National Football League, a disproportionate, and increasing, number of punters punt with their left leg, where punting is the position in play that receives and kicks the ball once it leaves the line of scrimmage. At the end of the 2017 NFL season, 10 out of the leagues 32 punters were left-footed, up from four out of 31 (not counting dual-footed punter Chris Hanson, who left the league in 2009) at the beginning of the millennium; in contrast, placekickers were almost exclusively right-footed. The only apparent advantage to punting with the left foot is that, because it is not as common, return specialists are not as experienced handling the ball spinning in the opposite direction.

Boardsports
In boardsports (e.g., surfing, skateboarding and snowboarding), one stands erect on a single, lightweight board that slides along the ground or on water. The need for balance causes one to position the body perpendicular to the direction of motion, with one foot leading the other. As with handedness, when this task is repetitively performed, one tends to naturally choose a particular foot for the leading position.

Goofy stance vs. regular stance
Boardsport riders are "footed" in one of two stances, generally called "regular" and "goofy". Riders will generally quickly choose a preferred stance that becomes permanently preferred. A "regular" stance indicates the left foot leading on the board with the right foot pushing, while a "Goofy" stance leads with the right foot on the board, pushing with the left. Professionals seem to be evenly distributed between the stances. Practice can yield a high level of ambidexterity between the two stances, such that even seasoned participants of a boardsport have difficulty discerning the footedness of an unfamiliar rider in action.
To increase the difficulty, variety, and aesthetic value of tricks, riders can ride "switch stance" (abbreviated to "switch"). For example, a goofy-footed skateboarder normally performs an ollie with the right foot forward, but a "switch ollie" would have the rider standing with the left foot at the front of the board. In sports where switch riding is common and expected, like street skateboarding, riders have the goal of appearing natural at, and performing the same tricks in, both regular and goofy stances. Some sports like kitesurfing and windsurfing generally require the rider to be able to switch stance depending on the wind or travel direction rather than rider preference. Each time direction is changed, the stance changes. Snowboarders who ride switch may adopt a "duck stance", where the feet are mounted turned out, or pointed away from the mid-line of the body, typically at a roughly 15-degree angle. In this position, the rider will have the leading foot facing forward in either regular or switch stance.

Switch, fakie and nollie
When a rider rolls backwards, this is called "riding fakie". A "fakie" trick is performed while riding backwards but taking off on the front foot. Although it is the same foot that jumps in ones traditional stance, it is normally the back foot. A rider can also land in the fakie position. While there are some parallels between switch stance and fakie, riding switch implies opening the shoulders more to face the direction headed, though not as much as in traditional stance, while fakie stance implies a slightly more backwards facing, closed shoulder posture. "Nollie" (nose ollie) is when the front foot takes off when one is riding in their normal stance, the same foot that jumps when doing tricks switch. In nollie position, the body and shoulders are facing forward as much as when riding in normal stance. Generally fakie and nollie are done off the nose, whereas normal and switch are done off the tail </s>