<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 Nightmare and can you explain it in depth? [/INST] A nightmare, also known as a bad dream, is an unpleasant dream that can cause a strong emotional response from the mind, typically fear but also despair, anxiety or great sadness. However, psychological nomenclature differentiates between nightmares and bad dreams; specifically, people remain asleep during bad dreams, whereas nightmares can awaken individuals. The dream may contain situations of discomfort, psychological or physical terror, or panic. After a nightmare, a person will often awaken in a state of distress and may be unable to return to sleep for a short period of time. Recurrent nightmares may require medical help, as they can interfere with sleeping patterns and cause insomnia.
Nightmares can have physical causes such as sleeping in an uncomfortable position or having a fever, or psychological causes such as stress or anxiety. Eating before going to sleep, which triggers an increase in the bodys metabolism and brain activity, can be a potential stimulus for nightmares.The prevalence of nightmares in children (5–12 years old) is between 20 and 30%, and for adults is between 8 and 30%. In common language, the meaning of nightmare has extended as a metaphor to many bad things, such as a bad situation or a scary monster or person.

Etymology
The word nightmare is derived from the Old English mare, a mythological demon or goblin who torments others with frightening dreams. The term has no connection with the Modern English word for a female horse. The word nightmare is cognate with the Dutch term nachtmerrie and German Nachtmahr (dated).
The sorcerous demons of Iranian mythology known as Divs are likewise associated with the ability to afflict their victims with nightmares.

Signs and symptoms
Those with nightmares experience abnormal sleep architecture. The impact of having a nightmare during the night has been found to be very similar to that of insomnia. This is thought to be caused by frequent nocturnal awakenings and fear of falling asleep. Nightmare disorder symptoms include repeated awakenings from the major sleep period or naps with detailed recall of extended and extremely frightening dreams, usually involving threats to survival, security, or self-esteem. The awakenings generally occur during the second half of the sleep period.

Classification
According to the International Classification of Sleep Disorders-Third Edition (ICSD-3), the nightmare disorder, together with REM sleep behaviour disorder (RBD) and recurrent isolated sleep paralysis, form the REM-related parasomnias subcategory of the Parasomnias cluster. Nightmares may be idiopathic without any signs of psychopathology or associated with disorders like stress, anxiety, substance abuse, psychiatric illness or PTSD (>80% of PTSD patients report nightmares). As regarding the dream content of the dreams they are usually imprinting negative emotions like sadness, fear or rage. According to the clinical studies the content can include being chased, injury or death of others, falling, natural disasters or accidents. Typical dreams or recurrent dreams may also have some of these topics.

Cause
Scientific research shows that nightmares may have many causes. In a study focusing on children, researchers were able to conclude that nightmares directly correlate with the stress in childrens lives. Children who experienced the death of a family member or a close friend or know someone with a chronic illness have more frequent nightmares than those who are only faced with stress from school or stress from social aspects of daily life.
A study researching the causes of nightmares focuses on patients who have sleep apnea. The study was conducted to determine whether or not nightmares may be caused by sleep apnea, or being unable to breathe. In the nineteenth century, authors believed that nightmares were caused by not having enough oxygen, therefore it was believed that those with sleep apnea had more frequent nightmares than those without it. The results actually showed that healthy people have more nightmares than sleep apnea patients.
Another study supports the hypothesis. In this study, 48 patients (aged 20–85 yrs) with obstructive airways disease (OAD), including 21 with and 27 without asthma, were compared with 149 sex- and age-matched controls without respiratory disease. OAD subjects with asthma reported approximately 3 times as many nightmares as controls or OAD subjects without asthma. The evolutionary purpose of nightmares then could be a mechanism to awaken a person who is in danger.
Lucid-dreaming advocate Stephen LaBerge has outlined a possible reason for how dreams are formulated and why nightmares occur. To LaBerge, a dream starts with an individual thought or scene, such as walking down a dimly lit street. Since dreams are not predetermined, the brain responds to the situation by either thinking a good thought or a bad thought, and the dream framework follows from there. If bad thoughts in a dream are more prominent than good thoughts, the dream may proceed to be a nightmare.There is a view, possibly featured in the story A Christmas Carol, that eating cheese before sleep can cause nightmares, but there is little scientific evidence for this.Severe nightmares are also likely to occur when person has a fever, these nightmares are often referred to as fever dreams.

Treatment
Sigmund Freud and Carl Jung seemed to have shared a belief that people frequently distressed by nightmares could be re-experiencing some stressful event from the past. Both perspectives on dreams suggest that therapy can provide relief from the dilemma of the nightmarish experience.
Halliday (1987) grouped treatment techniques into four classes. Direct nightmare interventions that combine compatible techniques from one or more of these classes may enhance overall treatment effectiveness:
Analytic and cathartic techniques
Storyline alteration procedures
Face-and-conquer approaches
Desensitization and related behavioral techniques

Post-traumatic stress disorder
Recurring post-traumatic stress disorder (PTSD) nightmares in which traumas are re-experienced respond well to a technique called imagery rehearsal. This involves dreamers coming up with alternative, mastery outcomes to the nightmares, mentally rehearsing those outcomes while awake, and then reminding themselves at bedtime that they wish these alternate outcomes should the nightmares reoccur. Research has found that this technique not only reduces the occurrence of nightmares and insomnia, but also improves other daytime PTSD symptoms. The most common variations of imagery rehearsal therapy (IRT) "relate to the number of sessions, duration of treatment, and the degree to which exposure therapy is included in the protocol".

Medication
Prazosin (alpha-1 blocker) appears useful in decreasing the number of nightmares and the distress caused by them in people with PTSD.
Risperidone (atypical antipsychotic) at a dosage of 2 mg per day, has been shown in case series to remission of nightmares on the first night.
Trazodone (antidepressant) has been shown in a case report to treat nightmares associated with a depressed patient.Trials have included hydrocortisone, gabapentin, paroxetine, tetrahydrocannabinol, eszopiclone, xyrem, and carvedilol.

See also
Bogeyman
False awakening
Hag § In folklore
Horror and terror
Mare (folklore)
Night terror
Nightmare disorder
Nocnitsa
Sleep disorder
Sleep paralysis
Succubus
Incubus
A Nightmare on Elm Street, 1984 film

References
Further reading
Anch, A. M.; Browman, C. P.; Mitler, M. M.; Walsh, J. K. (1988). Sleep: A Scientific Perspective. New Jersey: Prentice-Hall. ISBN 9780138129187.
Harris, J. C. (2004). "The Nightmare". Archives of General Psychiatry. 61 (5): 439–40. doi:10.1001/archpsyc.61.5.439. PMID 15123487.
Husser, J.-M.; Mouton, A., eds. (2010). Le Cauchemar dans les sociétés antiques. Actes des journées détude de lUMR 7044 (15–16 Novembre 2007, Strasbourg) (in French). Paris: De Boccard.
Jones, Ernest (1951). On the Nightmare. ISBN 978-0-87140-912-6.
Forbes, D.;  et al. (2001). "Brief Report: Treatment of Combat-Related Nightmares Using Imagery Rehearsal: A Pilot Study". Journal of Traumatic Stress. 14 (2): 433–442. doi:10.1023/A:1011133422340. PMID 11469167. S2CID 44630028.
Siegel, A. (2003). "A mini-course for clinicians and trauma workers on posttraumatic nightmares".
Burns, Sarah (2004). Painting the Dark Side : Art and the Gothic Imagination in Nineteenth-Century America. Ahmanson-Murphy Fine Are Imprint. University of California Press. ISBN 978-0-520-23821-3.
Davenport-Hines, Richard (1999). Gothic: Four Hundred Years of Excess, Horror, Evil and Ruin. North Point Press. pp. 160–61. ISBN 9780865475441.
Hill, Anne (2009). What To Do When Dreams Go Bad: A Practical Guide to Nightmares. Serpentine Media. ISBN 978-1-887590-04-4.
Simons, Ronald C.; Hughes, Charles C., eds. (1985). Culture-Bound Syndromes. Springer.
Sagan, Carl (1997). The Demon-Haunted World: Science as a Candle in the Dark.
Coalson, Bob (1995). "Nightmare help: Treatment of trauma survivors with PTSD". Psychotherapy: Theory, Research, Practice, Training. 32 (3): 381–388. doi:10.1037/0033-3204.32.3.381.
"Nightmares? Bad Dreams, or Recurring Dreams? Lucky You!". Archived from the original on 19 March 2012. Retrieved 8 December 2015.
Halliday, G. (1987). "Direct psychological therapies for nightmares: A review". Clinical Psychology Review. 7 (5): 501–523. doi:10.1016/0272-7358(87)90041-9.
Doctor, Ronald M.; Shiromoto, Frank N., eds. (2010). "Imagery Rehearsal Therapy (IRT)". The Encyclopedia of Trauma and Traumatic Stress Disorders </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 Nocturnal enuresis and can you explain it in depth? [/INST] Nocturnal enuresis, also informally called bedwetting, is involuntary urination while asleep after the age at which bladder control usually begins. Bedwetting in children and adults can result in emotional stress. Complications can include urinary tract infections.Most bedwetting is a developmental delay—not an emotional problem or physical illness. Only a small percentage (5 to 10%) of bedwetting cases have a specific medical cause. Bedwetting is commonly associated with a family history of the condition. Nocturnal enuresis is considered primary when a child has not yet had a prolonged period of being dry. Secondary nocturnal enuresis is when a child or adult begins wetting again after having stayed dry.
Treatments range from behavioral therapy, such as bedwetting alarms, to medication, such as hormone replacement, and even surgery such as urethral dilatation. Since most bedwetting is simply a developmental delay, most treatment plans aim to protect or improve self-esteem. Treatment guidelines recommend that the physician counsel the parents, warning about psychological consequences caused by pressure, shaming, or punishment for a condition children cannot control.Bedwetting is the most common childhood complaint.

Impact
A review of medical literature shows doctors consistently stressing that a bedwetting child is not at fault for the situation. Many medical studies state that the psychological impacts of bedwetting are more important than the physical considerations. "It is often the childs and family members reaction to bedwetting that determines whether it is a problem or not."

Self-esteem
Whether bedwetting causes low self-esteem remains a subject of debate, but several studies have found that self-esteem improved with management of the condition.Children questioned in one study ranked bedwetting as the third most stressful life event, after "parental war of words", divorce and parental fighting. Adolescents in the same study ranked bedwetting as tied for second with parental fighting.Bedwetters face problems ranging from being teased by siblings, being punished by parents, the embarrassment of still having to wear diapers, and being afraid that friends will find out.
Psychologists report that the amount of psychological harm depends on whether the bedwetting harms self-esteem or development of social skills. Key factors are:
How much the bedwetting limits social activities like sleep-overs and campouts
The degree of the social ostracism by peers
(Perceived) Anger, punishment, refusal and rejection by caregivers along with subsequent guilt
The number of failed treatment attempts
How long the child has been wetting

Behavioral impact
Studies indicate that children with behavioral problems are more likely to wet their beds. For children who have developmental problems, the behavioral problems and the bedwetting are frequently part of/caused by the developmental issues. For bedwetting children without other developmental issues, these behavioral issues can result from self-esteem issues and stress caused by the wetting.As mentioned below, current studies show that it is very rare for a child to intentionally wet the bed as a method of acting out.

Punishment for bedwetting
Medical literature states, and studies show, that punishing or shaming a child for bedwetting will frequently make the situation worse. It is best described as a downward cycle, where a child punished for bedwetting feels shame and a loss of self-confidence. This can cause increased bedwetting incidents, leading to more punishment and shaming.In the United States, about 25% of enuretic children are punished for wetting the bed. In Hong Kong, 57% of enuretic children are punished for wetting. Parents with only a grade-school level education punish bedwetting children at twice the rate of high-school- and college-educated parents.

Families
Parents and family members are frequently stressed by a childs bedwetting. Soiled linens and clothing cause additional laundry. Wetting episodes can cause lost sleep if the child wakes and/or cries, waking the parents. A European study estimated that a family with a child who wets nightly will pay about $1,000 a year for additional laundry, extra sheets, diapers, and mattress replacement.Despite these stressful effects, doctors emphasize that parents should react patiently and supportively.

Sociopathy
Bedwetting does not indicate a greater possibility of being a sociopath, as long as caregivers do not cause trauma by shaming or punishing a bedwetting child. Bedwetting was part of the Macdonald triad, a set of three behavioral characteristics described by John Macdonald in 1963.   The other two characteristics were firestarting and animal abuse.  Macdonald suggested that there was an association between a person displaying all three characteristics, then later displaying sociopathic criminal behavior.Up to 60% of multiple-murderers, according to some estimates, wet their beds post-adolescence.Enuresis is an "unconscious, involuntary [..] act".Bedwetting can be connected to past emotions and identity. Children under substantial stress, particularly in their home environment, frequently engage in bedwetting, in order to alleviate the stress produced by their surroundings. Trauma can also trigger a return to bedwetting (secondary enuresis) in both children and adults.
It is not bedwetting that increases the chance of criminal behavior, but the associated trauma. For example, parental cruelty can result in "homicidal proneness".

Causes
The aetiology of NE is not fully understood, although there are three common causes: excessive urine volume, poor sleep arousal, and bladder contractions. Differentiation of cause is mainly based on patient history and fluid charts completed by the parent or carer to inform management options.Bedwetting has a strong genetic component. Children whose parents were not enuretic have only a 15% incidence of bedwetting. When one or both parents were bedwetters, the rates jump to 44% and 77% respectively.These first two factors (aetiology and genetic component) are the most common in bedwetting, but current medical technology offers no easy testing for either cause. There is no test to prove that bedwetting is only a developmental delay, and genetic testing offers little or no benefit. As a result, other conditions should be ruled out. The following causes are less common, but are easier to prove and more clearly treated:In some bed-wetting children there is no increase in ADH (antidiuretic hormone) production, while other children may produce an increased amount of ADH but their response is insufficient.
Individuals with reported bedwetting issues are 2.7 times more likely to be diagnosed with Attention deficit hyperactivity disorder.
Caffeine increases urine production.
Chronic constipation can cause bed wetting. When the bowels are full, it can put pressure on the bladder. Often such children defecate normally, yet they retain a significant mass of material in the bowel which causes bed wetting.
Infections and disease are more strongly connected with secondary nocturnal enuresis and with daytime wetting. Less than 5% of all bedwetting cases are caused by infection or disease, the most common of which is a urinary tract infection.
Patients with more severe neurological-developmental issues have a higher rate of bedwetting problems. One study of seven-year-olds showed that "handicapped and intellectually disabled children" had a bedwetting rate almost three times higher than "non-handicapped children" (26.6% vs. 9.5%, respectively).
Psychological issues (e.g., death in the family, sexual abuse, extreme bullying) are established as a cause of secondary nocturnal enuresis (a return to bedwetting), but are very rarely a cause of PNE-type bedwetting. Bedwetting can also be a symptom of a pediatric neuropsychological disorder called PANDAS.
Sleep apnea stemming from an upper airway obstruction has been associated with bedwetting. Snoring and enlarged tonsils or adenoids are a sign of potential sleep apnea problems.
Sleepwalking can lead to bedwetting. During sleepwalking, the sleepwalker may think he/she is in another room. When the sleepwalker urinates during a sleepwalking episode, he/she usually thinks they are in the bathroom, and therefore urinate where they think the toilet should be. Cases of this have included opening a closet and urinating in it; urinating on the sofa and simply urinating in the middle of the room.
Stress is a cause of people who return to wetting the bed. Researchers find that moving to a new town, parent conflict or divorce, arrival of a new baby, or loss of a loved one or pet can cause insecurity, contributing to returning bedwetting.
Type 1 diabetes mellitus can first present as nocturnal enuresis.  It is classically associated with polyuria, polydipsia, and polyphagia; weight loss, lethargy, and diaper candidiasis may also be present in those with new-onset disease.

Unconfirmed
Food allergies may be part of the cause for some patients. This link is not well established, requiring further research.
Improper toilet training is another disputed cause of bedwetting. This theory was more widely supported in the last century and is still cited by some authors today. Some say bedwetting can be caused by improper toilet training, either by starting the training when the child is too young or by being too forceful. Recent research has shown more mixed results and a connection to toilet training has not been proven or disproven. According to the American Academy of Pediatrics, more child abuse occurs during potty training than in any other developmental stage.
Dandelions are reputed to be a potent diuretic, and anecdotal reports and folk wisdom say children who handle them can end up wetting the bed.  English folk names for the plant are "peebeds" and "pissabeds".  In French the dandelion is called pissenlit, which means "piss in bed"; likewise "piscialletto", an Italian folkname, and "meacamas" in Spanish.

Mechanism
Two physical functions prevent bedwetting. The first is a hormone that reduces urine production at night. The second is the ability to wake up when the bladder is full. Children usually achieve nighttime dryness by developing one or both of these abilities. There appear to be some hereditary factors in how and when these develop.The first ability is a hormone cycle that reduces the bodys urine production. At about sunset each day, the body releases a minute burst of antidiuretic hormone (also known as arginine vasopressin or AVP). This hormone burst reduces the kidneys urine output well into the night so that the bladder does not get full until morning. This hormone cycle is not present at birth. Many children develop it between the ages of two and six years old, others between six and the end of puberty, and some not at all.The second ability that helps people stay dry is waking when the bladder is full. This ability develops in the same age range as the vasopressin hormone, but is separate from that hormone cycle.
The typical development process begins with one- and two-year-old children developing larger bladders and beginning to sense bladder fullness. Two- and three-year-old children begin to stay dry during the day. Four- and five-year-olds develop an adult pattern of urinary control and begin to stay dry at night.

Diagnosis
Thorough history regarding frequency of bedwetting, any period of dryness in between, associated daytime symptoms, constipation, and encopresis should be sought.

Voiding diary
People are asked to observe, record and measure when and how much their child voids and drinks, as well as associated symptoms. A voiding diary in the form of a frequency volume chart records voided volume along with the time of each micturition for at least 24 hours. The frequency volume chart is enough for patients with complaints of nocturia and frequency only. If other symptoms are also present then a detailed bladder diary must be maintained. In a bladder diary, times of micturition and voided volume, incontinence episodes, pad usage, and other information such as fluid intake, the degree of urgency, and the degree of incontinence are recorded.

Physical examination
Each child should be examined physically at least once at the beginning of treatment. A full pediatric and neurological exam is recommended. Measurement of blood pressure is important to rule out any renal pathology. External genitalia and lumbosacral spine should be examined thoroughly.  A spinal defect, such as a dimple, hair tuft, or skin discoloration, might be visible in approximately 50% of patients with an intraspinal lesion. Thorough neurologic examination of the lower extremities, including gait, muscle power, tone, sensation, reflexes, and plantar responses should be done during first visit.

Classification
Nocturnal urinary continence is dependent on 3 factors: 1) nocturnal urine production, 2) nocturnal bladder function and 3) sleep and arousal mechanisms. Any child will experience nocturnal enuresis if more urine is produced than can be contained in the bladder or if the detrusor is hyperactive, provided that he or she is not awakened by the imminent bladder contraction.

Primary nocturnal enuresis
Primary nocturnal enuresis is the most common form of bedwetting. Bedwetting becomes a disorder when it persists after the age at which bladder control usually occurs (4–7 years), and is either resulting in an average of at least two wet nights a week with no long periods of dryness or not able to sleep dry without being taken to the toilet by another person.
New studies show that anti-psychotic drugs can have a side effect of causing enuresis.It has been shown that diet impacts enuresis in children. Constipation from a poor diet can result in impacted stool in the colon putting undue pressure on the bladder creating loss of bladder control (overflow incontinence).Some researchers, however, recommend a different starting age range. This guidance says that bedwetting can be considered a clinical problem if the child regularly wets the bed after turning 7 years old.

Secondary nocturnal enuresis
Secondary enuresis occurs after a patient goes through an extended period of dryness at night (six months or more) and then reverts to night-time wetting. Secondary enuresis can be caused by emotional stress or a medical condition, such as a bladder infection.

Psychological definition
Psychologists are usually allowed to diagnose and write a prescription for diapers if nocturnal enuresis causes the patient significant distress. Psychiatists may instead use a definition from the DSM-IV, defining nocturnal enuresis as repeated urination into bed or clothes, occurring twice per week or more for at least three consecutive months in a child of at least 5 years of age and not due to either a drug side effect or a medical condition.

Management
There are a number of management options for bedwetting. The following options apply when the bedwetting is not caused by a specifically identifiable medical condition such as a bladder abnormality or diabetes. Treatment is recommended when there is a specific medical condition such as bladder abnormalities, infection, or diabetes. It is also considered when bedwetting may harm the childs self-esteem or relationships with family/friends. Only a small percentage of bedwetting is caused by a specific medical condition, so most treatment is prompted by concern for the childs emotional welfare. Behavioral treatment of bedwetting overall tends to show increased self-esteem for children.Parents become concerned much earlier than doctors. A study in 1980 asked parents and physicians the age that children should stay dry at night. The average parent response was 2.75 years old, while the average physician response was 5.13 years old.Punishment is not effective and can interfere with treatment.

Treatment approaches
Simple behavioral methods are recommended as initial treatment. Other treatment methods include the following:

Motivational therapy in nocturnal enuresis mainly involves parent and child education. Guilt should be allayed by providing facts. Fluids should be restricted 2 hours prior to bed.  The child should be encouraged to empty the bladder completely prior to going to bed. Positive reinforcement can be initiated by setting up a diary or chart to monitor progress and establishing a system to reward the child for each night that they are dry. The child should participate in morning cleanup as a natural, nonpunitive consequence of wetting. This method is particularly helpful in younger children (<8 years) and will achieve dryness in 15-20% of the patients.
Waiting: Almost all children will outgrow bedwetting. For this reason, urologists and pediatricians frequently recommend delaying treatment until the child is at least six or seven years old. Physicians may begin treatment earlier if they perceive the condition is damaging the childs self-esteem and/or relationships with family/friends.
Bedwetting alarms: Physicians also frequently suggest bedwetting alarms which sound a loud tone when they sense moisture. This can help condition the child to wake at the sensation of a full bladder. These alarms are considered more effective than no treatment and may have a lower risk of adverse events than some medical therapies but it is still uncertain if alarms are more effective than other treatments. There may be a 29% to 69% relapse rate, so the treatment may need to be repeated.
DDAVP (desmopressin) tablets are a synthetic replacement for antidiuretic hormone, the hormone that reduces urine production during sleep. Desmopressin is usually used in the form of desmopressin acetate, DDAVP. Patients taking DDAVP are 4.5 times more likely to stay dry than those taking a placebo. The drug replaces the hormone for that night with no cumulative effect. US drug regulators have banned using desmopressin nasal sprays for treating bedwetting since the oral form is considered safer.
DDAVP is most efficient in children with nocturnal polyuria (nocturnal urine production greater than 130% of expected bladder capacity for age) and normal bladder reservoir function (maximum voided volume greater than 70% of expected bladder capacity for age). Other children who are likely candidates for desmopressin treatment are those in whom alarm therapy has failed or those considered unlikely to comply with alarm therapy. It can be very useful for summer camp and sleepovers to prevent enuresis.
Tricyclic antidepressants: Tricyclic antidepressant prescription drugs with anti-muscarinic properties have been proven successful in treating bedwetting, but also have an increased risk of side effects, including death from overdose. These drugs include amitriptyline, imipramine and nortriptyline. Studies find that patients using these drugs are 4.2 times as likely to stay dry as those taking a placebo. The relapse rates after stopping the medicines are close to 50%.

Condition management
Diapers: Wearing a diaper can reduce embarrassment for bedwetters and make cleanup easier for caregivers. These products are known as training pants or diapers when used for younger children, and as absorbent underwear or incontinence briefs when marketed for older children and adults. Some diapers are marketed especially for people with bedwetting. A major benefit is the reduced stress on both the bedwetter and caregivers. Wearing diapers can be especially beneficial for bedwetting children wishing to attend sleepovers or campouts, reducing emotional problems caused by social isolation and/or embarrassment in front of peers. According to one study of an adult with severe disabilities, extended diaper usage may interfere with learning to stay dry.
Waterproof mattress pads are used in some cases to ease clean-up of bedwetting incidents, however they only protect the mattress, and the sheets, bedding or sleeping partner may be soiled.

Unproven
Acupuncture: While acupuncture is safe in most adolescents, studies done to assess its effectiveness for nocturnal enuresis are of low quality.
Dry bed training: Dry bed training is frequently waking the child at night. Studies show this training is ineffective by itself and does not increase the success rate when used in conjunction with a bedwetting alarm.
Star chart: A star chart allows a child and parents to track dry nights, as a record and/or as part of a reward program. This can be done either alone or with other treatments. There is no research to show effectiveness, either in reducing bedwetting or in helping self-esteem. Some psychologists, however, recommend star charts as a way to celebrate successes and help a childs self-esteem.

Epidemiology
Doctors frequently consider bedwetting as a self-limiting problem, since most children will outgrow it </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 Onchocerciasis and can you explain it in depth? [/INST] Onchocerciasis, also known as river blindness, is a disease caused by infection with the parasitic worm Onchocerca volvulus. Symptoms include severe itching, bumps under the skin, and blindness. It is the second-most common cause of blindness due to infection, after trachoma.The parasite worm is spread by the bites of a black fly of the Simulium type. Usually, many bites are required before infection occurs. These flies live near rivers, hence the common name of the disease. Once inside a person, the worms create larvae that make their way out to the skin, where they can infect the next black fly that bites the person. There are a number of ways to make the diagnosis, including: placing a biopsy of the skin in normal saline and watching for the larva to come out; looking in the eye for larvae; and looking within the bumps under the skin for adult worms.A vaccine against the disease does not exist. Prevention is by avoiding being bitten by flies. This may include the use of insect repellent and proper clothing. Other efforts include those to decrease the fly population by spraying insecticides. Efforts to eradicate the disease by treating entire groups of people twice a year are ongoing in a number of areas of the world. Treatment of those infected is with the medication ivermectin every six to twelve months. This treatment kills the larvae but not the adult worms. The antibiotic doxycycline weakens the worms by killing an associated bacterium called Wolbachia, and is recommended by some as well. The lumps under the skin may also be removed by surgery.About 15.5 million people are infected with river blindness. Approximately 0.8 million have some amount of loss of vision from the infection. Most infections occur in sub-Saharan Africa, although cases have also been reported in Yemen and isolated areas of Central and South America. In 1915, the physician Rodolfo Robles first linked the worm to eye disease. It is listed by the World Health Organization (WHO) as a neglected tropical disease. In 2013 Colombia became first country to eradicate this disease.

Signs and symptoms
Adult worms remain in subcutaneous nodules, limiting access to the hosts immune system. Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. Wolbachia species have been found to be endosymbionts of O. volvulus adults and microfilariae, and are thought to be the driving force behind most of O. volvulus morbidity. Dying microfilariae have been recently discovered to release Wolbachia surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity.  The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response.Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has been developed to categorize the degree of skin involvement:
Acute papular onchodermatitis – scattered pruritic papules
Chronic papular onchodermatitis – larger papules, resulting in hyperpigmentation
Lichenified onchodermatitis – hyperpigmented papules and plaques, with edema, lymphadenopathy, pruritus and common secondary bacterial infections
Skin atrophy – loss of elasticity, the skin resembles tissue paper, lizard skin appearance
Depigmentation – leopard skin appearance, usually on anterior lower leg
Glaucoma effect – eyes malfunction, begin to see shadows or nothingOcular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve. The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms.The infected persons skin is itchy, with severe rashes permanently damaging patches of skin.

Mazzotti reaction
The Mazzotti reaction, first described in 1948, is a symptom complex seen in patients after undergoing treatment of onchocerciasis with the medication diethylcarbamazine (DEC). Mazzotti reactions can be life-threatening, and are characterized by fever, urticaria, swollen and tender lymph nodes, tachycardia, hypotension, arthralgias, oedema, and abdominal pain that occur within seven days of treatment of microfilariasis.

The phenomenon is so common when DEC is used that this drug is the basis of a skin patch test used to confirm that diagnosis. The drug patch is placed on the skin, and if the patient is infected with O. volvulus microfilaria, localized pruritus and urticaria are seen at the application site.

Nodding disease
This is an unusual form of epidemic epilepsy associated with onchocerciasis although definitive link has not been established. This syndrome was first described in Tanzania by Louise Jilek-Aall, a Norwegian psychiatric doctor in Tanzanian practice, during the 1960s. It occurs most commonly in Uganda and South Sudan. It manifests itself in previously healthy 5–15-year-old children, is often triggered by eating or low temperatures and is accompanied by cognitive impairment. Seizures occur frequently and may be difficult to control. The electroencephalogram is abnormal but cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) are normal or show non-specific changes. If there are abnormalities on the MRI they are usually present in the hippocampus. Polymerase chain reaction testing of the CSF does not show the presence of the parasite.

Cause
The cause is Onchocerca volvulus.

Life cycle
The life of the parasite can be traced through the black fly and the human hosts in the following steps:
A Simulium female black fly takes a blood meal on an infected human host, and ingests microfilaria.
The microfilaria enter the gut and thoracic flight muscles of the black fly, progressing into the first larval stage (J1.).
The larvae mature into the second larval stage (J2.), and move to the proboscis and into the saliva in its third larval stage (J3.). Maturation takes about seven days.
The black fly takes another blood meal, passing the larvae into the next human hosts blood.
The larvae migrate to the subcutaneous tissue and undergo two more molts.  They form nodules as they mature into adult worms over six to 12 months.
After maturing, adult male worms mate with female worms in the subcutaneous tissue to produce between 700 and 1,500 microfilaria per day.
The microfilaria migrate to the skin during the day, and the black flies only feed in the day, so the parasite is in a prime position for the female fly to ingest it. Black flies take blood meals to ingest these microfilaria to restart the cycle.

Diagnosis
Diagnosis can be made by skin biopsy (with or without PCR) or antibody testing.

Classification
Onchocerciasis causes different kinds of skin changes, which vary in different geographic regions; it may be divided into the following phases or types:: 440–441
Erisipela de la costa
An acute phase, it is characterized by swelling of the face, with erythema and itching.: 440  This skin change, erisípela de la costa, of acute onchocerciasis is most commonly seen among victims in Central and South America.Mal morando
This cutaneous condition is characterized by inflammation accompanied by hyperpigmentation.: 440
Sowda
A cutaneous condition, it is a localized type of onchocerciasis.: 440 Additionally, the various skin changes associated with onchocerciasis may be described as follows:: 440
Leopard skin
The spotted depigmentation of the skin that may occur with onchocerciasis: 440
Elephant skin
The thickening of human skin that may be associated with onchocerciasis: 440
Lizard skin
The thickened, wrinkled skin changes that may result with onchocerciasis: 441

Prevention
Various control programs aim to stop onchocerciasis from being a public health problem. The first was the Onchocerciasis Control Programme (OCP), which was launched in 1974, and at its peak, covered 30 million people in 11 countries. Through the use of larvicide spraying of fast-flowing rivers to control black fly populations, and from 1988 onwards, the use of ivermectin to treat infected people, the OCP eliminated onchocerciasis as a public health problem. The OCP, a joint effort of the World Health Organization, the World Bank, the United Nations Development Programme, and the UN Food and Agriculture Organization, was considered to be a success, and came to an end in 2002. Continued monitoring ensures onchocerciasis cannot reinvade the area of the OCP.

Elimination
In 1995, the African Programme for Onchocerciasis Control (APOC) began covering another 19 countries, mainly relying upon the use of the drug ivermectin. Its goal was to set up community-directed treatment with ivermectin for those at risk of infection. In these ways, transmission has declined. APOC closed in 2015 and aspects of its work taken over by the WHO Expanded Special Programme for the Elimination of Neglected Tropical Diseases (ESPEN). As in the Americas, the objective of ESPEN working with Government Health Ministries and partner NGDOs, is the elimination of transmission of onchocerciasis. This requires consistent annual treatment of 80% of the population in endemic areas for at least 10–12 years – the life span of the adult worm. No African country has so far verified elimination of onchocerciasis, but treatment has stopped in some areas (e.g. Nigeria), following epidemiological and entomological assessments that indicated that no ongoing transmission could be detected. In 2015, WHO facilitated the launch of an elimination program in Yemen which was subsequently put on hold due to conflict.In 1992, the Onchocerciasis Elimination Programme for the Americas, which also relies on ivermectin, was launched. On July 29, 2013, the Pan American Health Organization (PAHO) announced that after 16 years of efforts, Colombia had become the first country in the world to eliminate onchocerciasis. In September 2015, the Onchocerciasis Elimination Program for the Americas announced that onchocerciasis only remained in a remote region on the border of Brazil and Venezuela.  The area is home to the Yanomami indigenous people. The first countries to receive verification of elimination were Colombia in 2013, Ecuador in 2014, Mexico in 2015 and Guatemala in 2016. The key factor in elimination is mass administration of the antiparasitic drug ivermectin. The initial projection was that the disease would be eliminated from remaining foci in the Americas by 2012.No vaccine to prevent onchocerciasis infection in humans is available. A vaccine to prevent onchocerciasis infection for cattle is in phase three trials. Cattle injected with a modified and weakened form of O. ochengi larvae have developed very high levels of protection against infection.  The findings suggest that it could be possible to develop a vaccine that protects people against river blindness using a similar approach.  Unfortunately, a vaccine to protect humans is still many years off.

Treatment
In mass drug administration (MDA) programmes, the treatment for onchocerciasis is ivermectin (trade name: Mectizan); infected people can be treated with two doses of ivermectin, six months apart, repeated every three years. The drug paralyses and kills the microfilariae causing fever, itching, and possibly oedema, arthritis and lymphadenopathy. Intense skin itching is eventually relieved, and the progression towards blindness is halted. In addition, while the drug does not kill the adult worms, it does prevent them for a limited time from producing additional offspring. The drug therefore prevents both morbidity and transmission for up to several months.Ivermectin treatment is particularly effective because it only needs to be taken once or twice a year, needs no refrigeration, and has a wide margin of safety, with the result that it has been widely given by minimally trained community health workers.

Antibiotics
For the treatment of individuals, doxycycline is used to kill the Wolbachia bacteria that live in adult worms. This adjunct therapy has been shown to significantly lower microfilarial loads in the host, and may kill the adult worms, due to the symbiotic relationship between Wolbachia and the worm. In four separate trials over ten years with various dosing regimens of doxycycline for individualized treatment, doxycycline was found to be effective in sterilizing the female worms and reducing their numbers over a period of four to six weeks. Research on other antibiotics, such as rifampicin, has shown it to be effective in animal models at reducing Wolbachia both as an alternative and as an adjunct to doxycycline. However, doxycycline treatment requires daily dosing for at least four to six weeks, making it more difficult to administer in the affected areas.

Ivermectin
Ivermectin kills the parasite by interfering with the nervous system and muscle function, in particular, by enhancing inhibitory neurotransmission. The drug binds to and activates glutamate-gated chloride channels. These channels, present in neurons and myocytes, are not invertebrate-specific, but are protected in vertebrates from the action of ivermectin by the blood–brain barrier. Ivermectin is thought to irreversibly activate these channel receptors in the worm, eventually causing an inhibitory postsynaptic potential. The chance of a future action potential occurring in synapses between neurons decreases and the nematodes experience flaccid paralysis followed by death.Ivermectin is directly effective against the larval stage microfilariae of O. volvulus; they are paralyzed and can be killed by eosinophils and macrophages. It does not kill adult females (macrofilariae), but does cause them to cease releasing microfilariae, perhaps by paralyzing the reproductive tract. Ivermectin is very effective in reducing microfilarial load and reducing number of punctate opacities in individuals with onchocerciasis.

Moxidectin
Moxidectin was approved for onchocerciasis in 2018 for people over the age of 11 in the United States. The safety of multiple doses is unclear.

Epidemiology
About 21 million people were infected with this parasite in 2017; about 1.2 million of those had vision loss. As of 2017, about 99% of onchocerciasis cases occurred in Africa. Onchocerciasis is currently relatively common in 31 African countries, Yemen, and isolated regions of South America. Over 85 million people live in endemic areas, and half of these reside in Nigeria. Another 120 million people are at risk for contracting the disease. Due to the vectors breeding habitat, the disease is more severe along the major rivers in the northern and central areas of the continent, and severity declines in villages farther from rivers.  Onchocerciasis was eliminated in the northern focus in Chiapas, Mexico, and the focus in Oaxaca, Mexico, where Onchocerca volvulus existed, was determined, after several years of treatment with ivermectin, as free of the transmission of the parasite.According to a 2002 WHO report, onchocerciasis has not caused a single death, but its global burden is 987,000 disability adjusted life years (DALYs).  The severe pruritus alone accounts for 60% of the DALYs. Infection reduces the hosts immunity and resistance to other diseases, which results in an estimated reduction in life expectancy of 13 years.

History
Onchocerca originated in Africa and was exported to the Americas by the slave trade, as part of the Columbian exchange that introduced other old world diseases such as yellow fever into the New World. Findings of a phylogenetic study in the mid-90s are consistent with an introduction to the New World in this manner. DNA sequences of savannah and rainforest strains in Africa differ, while American strains are identical to savannah strains in western Africa. The microfilarial parasite that causes the disease was first identified in 1874 by an Irish naval surgeon, John ONeill, who was seeking to identify the cause of a common skin disease along the west coast of Africa, known as "craw-craw".  Rudolf Leuckart, a German zoologist, later examined specimens of the same filarial worm sent from Africa by a German missionary doctor in 1890 and named the organism Filaria volvulus.Rodolfo Robles and Rafael Pacheco in Guatemala first mentioned the ocular form of the disease in the Americas about 1915. They described a tropical worm infection with adult Onchocerca that included inflammation of the skin, especially the face (erisipela de la costa), and eyes. The disease, commonly called the "filarial blinding disease", and later referred to as "Robles disease", was common among coffee plantation workers. Manifestations included subcutaneous nodules, anterior eye lesions, and dermatitis. Robles sent specimens to Émile Brumpt, a French parasitologist, who named it O. caecutiens in 1919, indicating the parasite caused blindness (Latin "caecus" meaning blind). The disease was also reported as being common in Mexico.   By the early 1920s, it was generally agreed that the filaria in Africa and Central America were morphologically indistinguishable and the same as that described by ONeill 50 years earlier.Robles hypothesized that the vector of the disease was the day-biting black fly, Simulium. Scottish physician Donald Blacklock of the Liverpool School of Tropical Medicine confirmed this mode of transmission in studies in Sierra Leone. Blacklocks experiments included the re-infection of Simulium flies exposed to portions of the skin of infected subjects on which nodules were present, which led to elucidation of the life cycle of the Onchocerca parasite.  Blacklock and others could find no evidence of eye disease in Africa. Jean Hissette, a Belgian ophthalmologist,  discovered in 1930 that the organism was the cause of a "river blindness" in the Belgian Congo. Some of the patients reported seeing tangled threads or worms in their vision, which were microfilariae moving freely in the aqueous humor of the anterior chamber of the eye. Blacklock and Strong had thought the African worm did not affect the eyes, but Hissette reported that 50% of patients with onchocerciasis near the Sankuru river in the Belgian Congo had eye disease and 20% were blind. Hisette Isolated the microfilariae from an enucleated eye and described the typical chorioretinal scarring, later called the "Hissette-Ridley fundus" after another ophthalmologist, Harold Ridley, who also made extensive observations on onchocerciasis patients in north west Ghana, publishing his findings in  1945.  Ridley first postulated that the disease was brought by the slave trade. The international scientific community was initially skeptical of Hisettes findings, but they were confirmed by the Harvard African Expedition of 1934, led by Richard P. Strong, an American physician of tropical medicine.

Society and culture
Since 1987, ivermectin has been provided free of charge for use in humans by Merck through the Mectizan donation program (MDP). The MDP works together with ministries of health and nongovernmental development organisations, such as the World Health Organization, to provide free ivermectin to those who need it in endemic areas.In 2015 William C </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 Onychomycosis and can you explain it in depth? [/INST] Onychomycosis, also known as tinea unguium, is a fungal infection of the nail. Symptoms may include white or yellow nail discoloration, thickening of the nail, and separation of the nail from the nail bed. Toenails or fingernails may be affected, but it is more common for toenails. Complications may include cellulitis of the lower leg.
A number of different types of fungus can cause onychomycosis, including dermatophytes and Fusarium. Risk factors include athletes foot, other nail diseases, exposure to someone with the condition, peripheral vascular disease, and poor immune function. The diagnosis is generally suspected based on the appearance and confirmed by laboratory testing.Onychomycosis does not necessarily require treatment. The antifungal medication terbinafine taken by mouth appears to be the most effective but is associated with liver problems. Trimming the affected nails when on treatment also appears useful.There is a ciclopirox-containing nail polish, but there is no evidence that it works. The condition returns in up to half of cases following treatment. Not using old shoes after treatment may decrease the risk of recurrence.Onychomycosis occurs in about 10 percent of the adult population, with older people more frequently affected. Males are affected more often than females. Onychomycosis represents about half of nail disease. It was first determined to be the result of a fungal infection in 1853 by Georg Meissner.

Etymology
The term is from Ancient Greek ὄνυξ onyx "nail", μύκης mykēs "fungus", and the suffix -ωσις ōsis "functional disease".

Signs and symptoms
The most common symptom of a fungal nail infection is the nail becoming thickened and discoloured: white, black, yellow or green. As the infection progresses the nail can become brittle, with pieces breaking off or coming away from the toe or finger completely. If left untreated, the skin underneath and around the nail can become inflamed and painful. There may also be white or yellow patches on the nailbed or scaly skin next to the nail, and a foul smell. There is usually no pain or other bodily symptoms, unless the disease is severe. People with onychomycosis may experience significant psychosocial problems due to the appearance of the nail, particularly when fingers – which are always visible – rather than toenails are affected.Dermatophytids are fungus-free skin lesions that sometimes form as a result of a fungus infection in another part of the body. This could take the form of a rash or itch in an area of the body that is not infected with the fungus. Dermatophytids can be thought of as an allergic reaction to the fungus.

Causes
The causative pathogens of onychomycosis are all in the fungus kingdom and include dermatophytes, Candida (yeasts), and nondermatophytic molds. Dermatophytes are the fungi most commonly responsible for onychomycosis in the temperate western countries; while Candida and nondermatophytic molds are more frequently involved in the tropics and subtropics with a hot and humid climate.

Dermatophytes
When onychomycosis is due to a dermatophyte infection, it is termed tinea unguium. Trichophyton rubrum is the most common dermatophyte involved in onychomycosis. Other dermatophytes that may be involved are T. interdigitale, Epidermophyton floccosum, T. violaceum, Microsporum gypseum, T. tonsurans, and T. soudanense.  A common outdated name that may still be reported by medical laboratories is Trichophyton mentagrophytes for T. interdigitale. The name T. mentagrophytes is now restricted to the agent of favus skin infection of the mouse; though this fungus may be transmitted from mice and their danders to humans, it generally infects skin and not nails.

Other
Other causative pathogens include Candida and nondermatophytic molds, in particular members of the mold genus Scytalidium (name recently changed to Neoscytalidium), Scopulariopsis, and Aspergillus.
Candida species mainly cause fingernail onychomycosis in people whose hands are often submerged in water. Scytalidium mainly affects people in the tropics, though it persists if they later move to areas of temperate climate.
Other molds more commonly affect people older than 60 years, and their presence in the nail reflects a slight weakening in the nails ability to defend itself against fungal invasion.
Nail injury and nail psoriasis can cause damaged toenails to become thick, discolored & brittle.

Risk factors
Advancing age (usually over the age of 60) is the most common risk factor for onychomycosis due to diminished blood circulation, longer exposure to fungi, nails which grow more slowly and thicken, and reduced immune function increasing susceptibility to infection. Nail fungus tends to affect men more often than women and is associated with a family history of this infection.
Other risk factors include perspiring heavily, being in a humid or moist environment, psoriasis, wearing socks and shoes that hinder ventilation and do not absorb perspiration, going barefoot in damp public places such as swimming pools, gyms and shower rooms, having athletes foot (tinea pedis), minor skin or nail injury, damaged nail, or other infection, and having diabetes, circulation problems, which may also lead to lower peripheral temperatures on hands and feet, or a weakened immune system.

Diagnosis
The diagnosis is generally suspected based on the appearance and confirmed by laboratory testing. The four main tests are a potassium hydroxide smear, culture, histology examination, and polymerase chain reaction. The sample examined is generally nail scrapings or clippings. These being from as far up the nail as possible.Nail plate biopsy with periodic acid-Schiff stain appear more useful than culture or direct KOH examination. To reliably identify nondermatophyte molds, several samples may be necessary.

Classification
There are five classic types of onychomycosis:
Distal subungual onychomycosis is the most common form of tinea unguium and is usually caused by Trichophyton rubrum, which invades the nail bed and the underside of the nail plate.
White superficial onychomycosis (WSO) is caused by fungal invasion of the superficial layers of the nail plate to form "white islands" on the plate. It accounts for around 10 percent of onychomycosis cases. In some cases, WSO is a misdiagnosis of "keratins granulations" which are not a fungus, but a reaction to nail polish that can cause the nails to have a chalky white appearance. A laboratory test should be performed to confirm.
Proximal subungual onychomycosis is fungal penetration of the newly formed nail plate through the proximal nail fold. It is the least common form of tinea unguium in healthy people, but is found more commonly when the patient is immunocompromised.
Endonyx onychomycosis is characterized by leukonychia along with a lack of onycholysis or subungual hyperkeratosis.
Candidal onychomycosis is Candida species invasion of the fingernails, usually occurring in persons who frequently immerse their hands in water. This normally requires the prior damage of the nail by infection or trauma.

Differential diagnosis
In many cases of suspected nail fungus there is actually no fungal infection, but only nail deformity.To avoid misdiagnosis as nail psoriasis, lichen planus, contact dermatitis, nail bed tumors such as melanoma, trauma, or yellow nail syndrome, laboratory confirmation may be necessary.Other conditions that may appear similar to onychomycosis include: psoriasis, normal aging, yellow nail syndrome, and chronic paronychia.

Treatment
Medications
Most treatments are with antifungal medications, either topically or by mouth. Avoiding use of antifungal therapy by mouth (e.g., terbinafine) in persons without a confirmed infection is recommended, because of the possible side effects of that treatment.Medications that may be taken by mouth include terbinafine (76% effective), itraconazole (60% effective), and fluconazole (48% effective). They share characteristics that enhance their effectiveness: prompt penetration of the nail and nail bed, and persistence in the nail for months after discontinuation of therapy. Ketoconazole by mouth is not recommended due to side effects. Oral terbinafine is better tolerated than itraconazole. For superficial white onychomycosis, systemic rather than topical antifungal therapy is advised.Topical agents include ciclopirox nail paint, amorolfine, and efinaconazole. Some topical treatments need to be applied daily for prolonged periods (at least one year). Topical amorolfine is applied weekly.Efinaconazole, a topical azole antifungal, led to cure rates two or three times better than the next-best topical treatment, ciclopirox. In trials, about 17% of people were cured using efinaconazole, as opposed to 4% of people using placebo.Topical ciclopirox results in a cure in 6% to 9% of cases. Ciclopirox when used with terbinafine appears to be better than either agent alone. Although eficonazole, P-3051 (ciclopirox 8% hydrolacquer), and tavaborole are effective at treating fungal infection of toenails, complete cure rates are low.

Other
Chemical (keratolytic) or surgical debridement of the affected nail appears to improve outcomes.As of 2014 evidence for laser treatment is unclear as the evidence is of low quality and varies by type of laser.Tea tree oil is not recommended as a treatment, since it is not effective and can irritate the surrounding skin.

Cost
United States
According to a 2015 study, the cost in the United States of testing with the periodic acid–Schiff stain (PAS) was about $148. Even if the cheaper KOH test is used first and the PAS test is used only if the KOH test is negative, there is a good chance that the PAS will be done (because of either a true or a false negative with the KOH test). But the terbinafine treatment costs only $10 (plus an additional $43 for liver function tests). In conclusion the authors say that terbinafine has a relatively benign adverse effect profile, with liver damage very rare, so it makes more sense cost-wise for the dermatologist to prescribe the treatment without doing the PAS test. (Another option would be to prescribe the treatment only if the potassium hydroxide test is positive, but it gives a false negative in about 20% of cases of fungal infection.) On the other hand, as of 2015 the price of topical (non-oral) treatment with efinaconazole was $2307 per nail, so testing is recommended before prescribing it.The cost of efinaconazole treatment can be reduced to $65 per 1-month dose using drug coupons, bringing the treatment cost to $715 per nail.

Canada
In 2019, a study by the Canadian Agency for Drugs and Technologies in Health found the cost for a 48-week efinaconazole course to be $178 for a big toe, and $89 for an other toe.

Prognosis
Recurrence may occur following treatment, with a 20-25% relapse rate within 2 years of successful treatment. Nail fungus can be painful and cause permanent damage to nails </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 Neonatal conjunctivitis and can you explain it in depth? [/INST] Neonatal conjunctivitis is a form of conjunctivitis (inflammation of the outer eye) which affects newborn babies following birth. It is typically due to neonatal bacterial infection, although can also be non-infectious (e.g. chemical exposure). Infectious neonatal conjunctivitis is typically contracted during vaginal delivery from exposure to bacteria from the birth canal, most commonly Neisseria gonorrhoeae or Chlamydia trachomatis.Antibiotic ointment is typically applied to the newborns eyes within 1 hour of birth as prevention for gonococcal ophthalmia. This practice is recommended for all newborns and most hospitals in the United States are required by state law to apply eye drops or ointment soon after birth to prevent the disease.If left untreated, neonatal conjunctivitis can cause blindness.

Signs and symptoms
Neonatal conjunctivitis by definition presents during the first month of life. Signs and symptoms include:
Pain and tenderness in the eyeball
Conjunctival discharge: purulent, mucoid or mucopurulent (depending on the cause)
Conjunctival hyperaemia and chemosis, usually also with swelling of the eyelids
Corneal involvement (rare) may occur in herpes simplex ophthalmia neonatorum

Time of onset
Chemical causes: Right after delivery
Neisseria gonorrhoeae: Delivery of the baby until 5 days after birth (early onset)
Chlamydia trachomatis: 5 days after birth to 2 weeks (late onset – C. trachomatis has a longer incubation period)

Complications
Untreated cases may develop corneal ulceration, which may perforate, resulting in corneal opacification and staphyloma formation.

Cause
Non-infectious
Chemical irritants such as silver nitrate can cause chemical conjunctivitis, usually lasting 2–4 days. Thus, prophylaxis with a 1% silver nitrate solution is no longer in common use. In most countries, neomycin and chloramphenicol eye drops are used, instead.
However, newborns can develop neonatal conjunctivitis due to reactions with chemicals in these common eye drops. Additionally, a blocked tear duct may be another noninfectious cause of neonatal conjunctivitis.

Infectious
The two most common infectious causes of neonatal conjunctivitis are N. gonorrheae and Chlamydia, typically acquired from the birth canal during delivery. However, other different bacteria and viruses can be the cause, including herpes simplex virus (HSV 2), Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus pneumoniae.Ophthalmia neonatorum due to gonococci (N. gonorrhoeae) typically manifests in the first 5 days after birth and is associated with marked bilateral purulent discharge and local inflammation. In contrast, conjunctivitis secondary to infection with C. trachomatis produces conjunctivitis 3 days to 2 weeks after delivery. The discharge is usually more watery in nature (mucopurulent) and less inflamed </s>