<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Dermatitis and explain in detail? [/INST] Dermatitis is inflammation of the skin, typically characterized by itchiness, redness and a rash. In cases of short duration, there may be small blisters, while in long-term cases the skin may become thickened. The area of skin involved can vary from small to covering the entire body. Dermatitis is often called eczema, and the difference between those terms is not standardized.
The exact cause of the condition is often unclear. Cases may involve a combination of  allergy and poor venous return. The type of dermatitis is generally determined by the persons history and the location of the rash. For example, irritant dermatitis often occurs on the hands of those who frequently get them wet. Allergic contact dermatitis occurs upon exposure to an allergen, causing a hypersensitivity reaction in the skin.Prevention of atopic dermatitis is typically with essential fatty acids, and may be treated with moisturizers and steroid creams. The steroid creams should generally be of mid- to high strength and used for less than two weeks at a time, as side effects can occur. Antibiotics may be required if there are signs of skin infection. Contact dermatitis is typically treated by avoiding the allergen or irritant. Antihistamines may help with sleep and decrease nighttime scratching.Dermatitis was estimated to affect 245 million people globally in 2015, or 3.34% of the world population. Atopic dermatitis is the most common type and generally starts in childhood. In the United States, it affects about 10–30% of people. Contact dermatitis is twice as common in females as males. Allergic contact dermatitis affects about 7% of people at some point in their lives. Irritant contact dermatitis is common, especially among people with certain occupations; exact rates are unclear.

Types
Dermatitis includes:
Atopic dermatitis
Allergic contact dermatitis
Irritant contact dermatitis
Seborrhoeic dermatitis
Stasis dermatitis

Signs and symptoms
Dermatitis symptoms vary with all different forms of the condition. Although every type of dermatitis has different symptoms, there are certain signs that are common for all of them, including redness of the skin, swelling, itching and skin lesions with sometimes oozing and scarring. Also, the area of the skin on which the symptoms appear tends to be different with every type of dermatitis, whether on the neck, wrist, forearm, thigh or ankle. Although the location may vary, the primary symptom of this condition is itchy skin. More rarely, it may appear on the genital area, such as the vulva or scrotum. Symptoms of this type of dermatitis may be very intense and may come and go. Irritant contact dermatitis is usually more painful than itchy.
Although the symptoms of atopic dermatitis vary from person to person, the most common symptoms are dry, itchy, red skin. Typical affected skin areas include the folds of the arms, the back of the knees, wrists, face and hands. Perioral dermatitis refers to a red bumpy rash around the mouth.Dermatitis herpetiformis symptoms include itching, stinging and a burning sensation. Papules and vesicles are commonly present. The small red bumps experienced in this type of dermatitis are usually about 1 cm in size, red in color and may be found symmetrically grouped or distributed on the upper or lower back, buttocks, elbows, knees, neck, shoulders and scalp.
The symptoms of seborrhoeic dermatitis, on the other hand, tend to appear gradually, from dry or greasy scaling of the scalp (dandruff) to scaling of facial areas, sometimes with itching, but without hair loss.  In newborns, the condition causes a thick and yellowish scalp rash, often accompanied by a diaper rash. In severe cases, symptoms may appear along the hairline, behind the ears, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.

Complications
People with eczema should not receive the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.
Other major health risks for people with dermatitis are viral and bacterial infections because atopic dermatitis patients have deficiencies in their proteins and lipids that have barrier functions along with defects in dendritic cells and as a result are unable to keep foreign invaders out leading to recurring infections. If left untreated, these infections may be life-threatening, so skin barrier improvement (such as daily moisturizing to minimize transepidermal water loss) and anti-inflammatory therapy are recommended as preventative measures.

Cause
The cause of dermatitis is unknown but is presumed to be a combination of genetic and environmental factors.

Environmental
The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment in childhood which leads to an insufficient human microbiota. It is supported by epidemiologic studies for asthma. The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases the risk for asthma and allergy. One systematic review of literature on eczema found that urban areas have an increased prevalence of eczema compared to rural areas.
While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites, with up to 5% of people showing antibodies to the mites, the overall role this plays awaits further corroboration.

Malnutrition
Essential fatty acid deficiency results in a dermatitis similar to that seen in zinc or biotin deficiency.

Genetic
A number of genes have been associated with eczema, one of which is filaggrin. Genome-wide studies found three new genetic variants associated with eczema: OVOL1, ACTL9 and IL4-KIF3A.Eczema occurs about three times more frequently in individuals with celiac disease and about two times more frequently in relatives of those with celiac disease, potentially indicating a genetic link between the conditions.

Prevention
Exclusive breastfeeding of infants during at least the first few months may decrease the risk. There is no good evidence that a mothers diet during pregnancy or breastfeeding affects the risk, nor is there evidence that delayed introduction of certain foods is useful. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use. There is moderate certainty evidence that the use of skin care interventions such as emollients within the first year of life of an infants life is not effective in preventing eczema. In fact, it may increase the risk of skin infection and of unwanted effects such as allergic reaction to certain moisturizers and a stinging sensation.

Healthy diet
There has not been adequate evaluation of changing the diet to reduce eczema. There is some evidence that infants with an established egg allergy may have a reduction in symptoms if eggs are eliminated from their diets. Benefits have not been shown for other elimination diets, though the studies are small and poorly executed. Establishing that there is a food allergy before dietary change could avoid unnecessary lifestyle changes.

Fatty acids
Oils with fatty acids that has been studied to prevent dermatitis includes:
Corn oil: Linoleic acid (LA)
Fish oil: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)
Hemp seed oil: Linoleic acid (LA), and alpha-Linolenic acid (ALA)In the 1950s Arild Hansen showed that in humans: infants fed skimmed milk developed the essential fatty acid deficiency. It was characterized by an increased food intake, poor growth, and a scaly dermatitis, and was cured by the administration of corn oil.

Management
There is no known cure for some types of dermatitis, with treatment aiming to control symptoms by reducing inflammation and relieving itching. Contact dermatitis is treated by avoiding what is causing it.

Lifestyle
Bathing once or more a day is recommended, usually for five to ten minutes in warm water. Soaps should be avoided, as they tend to strip the skin of natural oils and lead to excessive dryness. The American Academy of Dermatology suggests using a controlled amount of bleach diluted in a bath to help with atopic dermatitis.People can wear clothing designed to manage the itching, scratching and peeling.House dust mite reduction and avoidance measures have been studied in low quality trials and have not shown evidence of improving eczema.

Moisturizers
Low-quality evidence indicates that moisturizing agents (emollients) may reduce eczema severity and lead to fewer flares. In children, oil–based formulations appear to be better, and water–based formulations are not recommended. It is unclear if moisturizers that contain ceramides are more or less effective than others. Products that contain dyes, perfumes, or peanuts should not be used. Occlusive dressings at night may be useful.Some moisturizers or barrier creams may reduce irritation in occupational irritant hand dermatitis, a skin disease that can affect people in jobs that regularly come into contact with water, detergents, chemicals or other irritants. Some emollients may reduce the number of flares in people with dermatitis.

Medications
Corticosteroids
If symptoms are well controlled with moisturizers, steroids may only be required when flares occur. Corticosteroids are effective in controlling and suppressing symptoms in most cases. Once daily use is generally enough. For mild-moderate eczema a weak steroid may be used (e.g., hydrocortisone), while in more severe cases a higher-potency steroid (e.g., clobetasol propionate) may be used. In severe cases, oral or injectable corticosteroids may be used. While these usually bring about rapid improvements, they have greater side effects.
Long term use of topical steroids may result in skin atrophy, stria, telangiectasia. Their use on delicate skin (face or groin) is therefore typically with caution. They are, however, generally well tolerated. Red burning skin, where the skin turns red upon stopping steroid use, has been reported among adults who use topical steroids at least daily for more than a year.

Antihistamines
There is little evidence supporting the use of antihistamine medications for the relief of dermatitis. Sedative antihistamines, such as diphenhydramine, may be useful in those who are unable to sleep due to eczema. Second generation antihistamines have minimal evidence of benefit. Of the second generation antihistamines studied, fexofenadine is the only one to show evidence of improvement in itching with minimal side effects.

Immunosuppressants
Topical immunosuppressants like pimecrolimus and tacrolimus may be better in the short term and appear equal to steroids after a year of use. Their use is reasonable in those who do not respond to or are not tolerant of steroids. Treatments are typically recommended for short or fixed periods of time rather than indefinitely. Tacrolimus 0.1% has generally proved more effective than pimecrolimus, and equal in effect to mid-potency topical steroids. There is no link to increased risk of cancer from topical use of 1% pimecrolimus cream.When eczema is severe and does not respond to other forms of treatment, systemic immunosuppressants are sometimes used. Immunosuppressants can cause significant side effects and some require regular blood tests. The most commonly used are ciclosporin, azathioprine, and methotrexate.
Dupilumab is a new medication that improves eczema lesions, especially moderate to severe eczema. Dupilumab, a monoclonal antibody, suppresses inflammation by targeting the interleukin-4 receptor.

Others
In September 2021, ruxolitinib cream (Opzelura) was approved by the U.S. Food and Drug Administration (FDA) for the topical treatment of mild to moderate atopic dermatitis. It is a topical Janus kinase inhibitor.

Light therapy
Narrowband UVB
Atopic dermatitis (AD) may be treated with narrowband UVB, which increases 25-hydroxyvitamin D3 in persons in individuals with AD.Light therapy using heliotherapy, balneophototherapy, psoralen plus UVA (PUVA), light has tentative support but the quality of the evidence is not very good compared with narrowband UVB, and UVA1. However, UVB is more effective than UVA1 for treatment of atopical dermatitis.Overexposure to ultraviolet light carries its own risks, particularly that of skin cancer.

Alternative medicine
Topical
Limited evidence suggests that acupuncture may reduce itching in those affected by atopic dermatitis.Chiropractic spinal manipulation lacks evidence to support its use for dermatitis. There is little evidence supporting the use of psychological treatments. While dilute bleach baths have been used for infected dermatitis there is little evidence for this practice.

Supplements
Sulfur: There is currently no scientific evidence for the claim that sulfur treatment relieves eczema.
Chinese herbs: It is unclear whether Chinese herbs help or harm. Dietary supplements are commonly used by people with eczema.
Neither evening primrose oil nor borage seed oil taken orally have been shown to be effective. Both are associated with gastrointestinal upset.
Probiotics are likely to make little to no difference in symptoms.

Pathophysiology
Eczema can be characterized by spongiosis which allows inflammatory mediators to accumulate. Different dendritic cells sub types, such as Langerhans cells, inflammatory dendritic epidermal cells and plasmacytoid dendritic cells have a role to play.

Diagnosis
Diagnosis of eczema is based mostly on the history and physical examination. In uncertain cases, skin biopsy may be taken for a histopathologic diagnosis of dermatitis. Those with eczema may be especially prone to misdiagnosis of food allergies.Patch tests are used in the diagnosis of allergic contact dermatitis.

Classification
The term eczema refers to a set of clinical characteristics. Classification of the underlying diseases has been haphazard with numerous different classification systems, and many synonyms being used to describe the same condition.A type of dermatitis may be described by location (e.g., hand eczema), by specific appearance (eczema craquele or discoid) or by possible cause (varicose eczema). Further adding to the confusion, many sources use the term eczema interchangeably for the most common type: atopic dermatitis.The European Academy of Allergology and Clinical Immunology (EAACI) published a position paper in 2001, which simplifies the nomenclature of allergy-related diseases, including atopic and allergic contact eczemas. Non-allergic eczemas are not affected by this proposal.

Histopathologic classification
By histopathology, superficial dermatitis (in the epidermis, papillary dermis, and superficial vascular plexus) can basically be classified into either of the following groups:
Vesiculobullous lesions
Pustular dermatosis
Non vesicullobullous, non-pustularWith epidermal changes
Without epidermal changes. These characteristically have a superficial perivascular inflammatory infiltrate and can be classified by type of cell infiltrate:Lymphocytic (most common)
Lymphoeosinophilic
Lymphoplasmacytic
Mast cell
Lymphohistiocytic
Neutrophilic

Terminology
There are several types of dermatitis including atopic dermatitis, contact dermatitis, stasis dermatitis and seborrhoeic dermatitis. Many authors use the terms dermatitis and eczema synonymously, and various dictionaries that treat the terms as differentiable nonetheless do not provide explicit criteria for differentiating them, as the aspects of inflammation, pruritus, and either exogenous or endogenous provoking agent all can apply to either term, and thus autoimmune components are not excluded from either.
Others use the term eczema to specifically mean atopic dermatitis. Atopic dermatitis is also known as atopic eczema. In some languages, dermatitis and eczema mean the same thing, while in other languages dermatitis implies an acute condition and eczema a chronic one.

Common types
Diagnosis of types may be indicated by codes defined according to International Statistical Classification of Diseases and Related Health Problems (ICD).

Atopic
Atopic dermatitis is an allergic disease believed to have a hereditary component and often runs in families whose members have asthma. Itchy rash is particularly noticeable on the head and scalp, neck, inside of elbows, behind knees, and buttocks. It is very common in developed countries and rising. Irritant contact dermatitis is sometimes misdiagnosed as atopic dermatitis. Stress can cause atopic dermatitis to worsen.

Contact
Contact dermatitis is of two types: allergic (resulting from a delayed reaction to an allergen, such as poison ivy, nickel, or Balsam of Peru), and irritant (resulting from direct reaction to a detergent, such as sodium lauryl sulfate, for example).
Some substances act both as allergen and irritants (wet cement, for example). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis. About three-quarters of cases of contact eczema are of the irritant type, which is the most common occupational skin disease. Contact eczema is curable, provided the offending substance can be avoided and its traces removed from ones environment. (ICD-10 L23; L24; L56.1; L56.0)

Seborrhoeic
Seborrhoeic dermatitis or seborrheic dermatitis is a condition sometimes classified as a form of eczema that is closely related to dandruff. It causes dry or greasy peeling of the scalp, eyebrows, and face, and sometimes trunk. In newborns, it causes a thick, yellow, crusty scalp rash called cradle cap, which seems related to lack of biotin and is often curable. (ICD-10 L21; L21.0)

Less common types
Dyshidrosis
Dyshidrosis (dyshidrotic eczema, pompholyx, vesicular palmoplantar dermatitis) only occurs on palms, soles, and sides of fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching, which gets worse at night. A common type of hand eczema, it worsens in warm weather. (ICD-10 L30.1)

Discoid
Discoid eczema (nummular eczema, exudative eczema, microbial eczema) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. The cause is unknown, and the condition tends to come and go. (ICD-10 L30.0)

Venous
Venous eczema (gravitational eczema, stasis dermatitis, varicose eczema) occurs in people with impaired circulation, varicose veins, and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin, and itching. The disorder predisposes to leg ulcers. (ICD-10 I83.1)

Herpetiformis
Dermatitis herpetiformis (Duhrings disease) causes an intensely itchy and typically symmetrical rash on arms, thighs, knees, and back. It is directly related to celiac disease, can often be put into remission with an appropriate diet, and tends to get worse at night. (ICD-10 L13.0)

Neurodermatitis
Neurodermatitis (lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch that results from habitual rubbing and scratching. Usually, there is only one spot. Often curable through behaviour modification and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps. (ICD-10 L28.0; L28.1)

Autoeczematization
Autoeczematization (id reaction, auto sensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria, or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending on the cause. It always occurs some distance away from the original infection. (ICD-10 L30.2)

Viral
There are eczemas overlaid by viral infections (eczema herpeticum or vaccinatum), and eczemas resulting from underlying disease (e.g., lymphoma).
Eczemas originating from ingestion of medications, foods, and chemicals, have not yet been clearly systematized. Other rare eczematous disorders exist in addition to those listed here.

Prognosis
Most cases are well managed with topical treatments and ultraviolet light. About 2% of cases are not. In more than 60% of young children, the condition subsides by adolescence.

Epidemiology
Globally dermatitis affected approximately 230 million people as of 2010 (3.5% of the population). Dermatitis is most commonly seen in infancy, with female predominance of eczema presentations occurring during the reproductive period of 15–49 years. In the UK about 20% of children have the condition, while in the United States about 10% are affected.Although little data on the rates of eczema over time exists prior to the 1940s, the rate of eczema has been found to have increased substantially in the latter half of the 20th century, with eczema in school-aged children being found to increase between the late 1940s and 2000. In the developed world there has been rise in the rate of eczema over time.  The incidence and lifetime prevalence of eczema in England has been seen to increase in recent times.Dermatitis affected about 10% of U.S </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Macropsia and explain in detail? [/INST] Macropsia is a neurological condition affecting human visual perception, in which objects within an affected section of the visual field appear larger than normal, causing the person to feel smaller than they actually are. Macropsia, along with its opposite condition, micropsia, can be categorized under dysmetropsia. Macropsia is related to other conditions dealing with visual perception, such as aniseikonia and Alice in Wonderland Syndrome (AIWS, also known as Todds syndrome).  Macropsia has a wide range of causes, from prescription and illicit drugs, to migraines and (rarely) complex partial epilepsy, and to different retinal conditions, such as epiretinal membrane. Physiologically, retinal macropsia results from the compression of cones in the eye. It is the compression of receptor distribution that results in greater stimulation and thus a larger perceived image of an object.

Signs and symptoms
The most obvious symptom of macropsia is the presence of exceptionally enlarged objects throughout the visual field. For example, a young girl might see her sisters books as the same size as her sister. Stemming from this symptom, someone with macropsia may feel undersized in relation to his or her surrounding environment. Patients with macropsia have also noted the cessation of auditory function prior to the onset of visual hallucination, indicating possible seizure either before or after the hallucination. A buzzing sound in the ears has also been reported immediately before macropsia development. Some patients claim that symptoms may be eased if an attempt is made to physically touch the object which appears enormous in size. It is important to note, however, that patients typically remain lucid and alert throughout episodes, being able to recount specific details. A person with macropsia may have no psychiatric conditions. Symptoms caused chemically by drugs such as cannabis, magic mushrooms, or cocaine tend to dissipate after the chemical compound has been excreted from the body. Those who acquire macropsia as a symptom of a virus usually experience complete recovery and restoration of normal vision.Dysmetropsia in one eye, a case of aniseikonia, can present with symptoms such as headaches, asthenopia, reading difficulties, depth perception problems, or double vision. The visual distortion can cause uncorrelated images to stimulate corresponding retinal regions simultaneously impairing fusion of the images. Without suppression of one of the images symptoms from mild poor stereopsis, binocular diplopia and intolerable rivalry can occur.

Psychological effects
There are a broad range of psychological and emotional effects that a person with macropsia may experience. One competing theory has radically stated that macropsia may be an entirely psychological pathological phenomenon without any structural defect or definite cause. They may be in an irritable or angry state, or in contrast, a euphoric state. There is evidence that those who experience Alice in Wonderland Syndrome and associated macropsia are able to recount their experiences with thorough detail. There may be no evidence of psychiatric disturbance and, as a result, no psychiatric therapy may be required. Psychological conditions often arise from macropsia, but the general consensus is that they do not cause macropsia. Those affected may experience extreme anxiety both during and after episodes as a result of the overwhelming nature of his or her distorted visual field. Due to the fear and anxiety associated with the condition, those who have previously had an episode hesitate to recount the episode, although retain the ability to do so. Psychologically, a person with macropsia may feel separation and dissociation from the outside world and even from immediate family. This feeling of dissociation has mostly been noted in child or adolescent patients. The patient may feel that he or she must unfairly contend with hostile and aggressive forces due to the gigantic nature of the surrounding environment. The defense against said forces is usually expressed verbally. The patient may falsely present an outgoing or flamboyant persona, while remaining fearful of people internally. He or she, in an attempt to balance the size distortion, may try to make others feel small in size through insult or hostile behavior. The psychological impact of macropsia on long-time people who have had the condition since childhood may be greater and lead to severe ego-deficiencies. An alternative interpretation of the condition is that macropsia is a response to biophysiological contraction and has no psychological roots. Thus, when a patient reaches for an enlarged object, he or she is overcoming that physiological contraction. However, this theory has been under much scrutiny.

Causes
Structural defects
In cases where macropsia affects one eye resulting in differences in the way the two eyes perceive the size or shape of images, the condition is known as aniseikonia. Aniseikonia is known to be associated with certain retinal conditions. Epiretinal membrane has been found to cause metamorphopsia and aniseikonia. Vitreomacular traction caused by the excessive adhesion of vitreous fluid to the retina is related to aniseikonia due to the separation and compression of photoreceptor cells. Macular edema and surgical re-attachment for macula-off rhegmatogenous retinal detachment can also cause an increased separation of macular photoreceptor cells resulting in dysmetropsia. Retinoschisis is another eye disease that has been shown to cause aniseikonia.There is evidence that a lesion appearing in the posterior area of the ventral occipitotemporal visual pathway can cause macropsia. This lesion can be due to an ischemic cell death after an acute posterior cerebral infarction.

Medications
The most prevalent research on prescription drugs with side effects of macropsia deals with zolpidem and citalopram. Zolpidem is a drug prescribed for insomnia, and although it has proven beneficial effects, there have been numerous reported cases of adverse perceptual reactions. One of these cases discusses an anorexic womans episode of macropsia, which occurred twenty minutes after taking 10 mg zolpidem. The same woman later had two more episodes of zolpidem-induced macropsia, after taking 5 mg and 2.5 mg zolpidem, respective to each episode. The intensity of the macropsia episodes decreased with the decreasing amount of zolpidem administered; it is implied in the article that the level of intensity was based on the patients accounts of her macropsia episodes, and that no external diagnosis was used. Hoyler points out notable similarities among the different reported cases of zolpidem-induced disorganization. The similarities were that all the cases were reported by women, the disorganization and agitation followed the first administration of zolpidem, and once zolpidem was discontinued, there were no lasting residual effects. It is believed that zolpidem-related macropsia is more prevalent in women because plasma zolpidem concentration is 40% higher in women, a concentration that further increases in anorexic women.Citalopram-induced macropsia is similar to zolpidem-induced macropsia since both types have been observed in relatively few cases, and neither of the drugs side effects can be supported by experimental evidence. Citalopram is an antidepressant that inhibits serotonin reuptake. The first case of macropsia thought to be induced by citalopram involves a woman who experienced macropsia after her first administration of 10 mg citalopram. Just as with zolpidem, after the immediate discontinuation of citalopram, there were no further episodes of macropsia.

Illicit drugs
There are suggestions that visual distortions, such as macropsia, can be associated with cocaine use. Episodes of temporary drug-induced macropsia subside as the chemicals leave the body.

Migraine
Past research has linked macropsia to migraine. One of these studies was conducted on Japanese adolescents who reported visual episodic illusions with macropsia and showed that illusions are three times more likely to occur in association with migraine. The illusions were most prevalent among girls between the ages of 16 and 18. It is unlikely that macropsia in Japanese adolescents could be due to epileptic seizure since only 0.3% of Japanese adolescents have epilepsy. No evidence of drugs was found, which eliminates the possibility of the macropsia in the adolescents being drug-induced. It is also unlikely for macropsia in adolescent children to be associated with a serious disease. It is usually the macropsia or other visual disturbance which precedes the painful migrainous headaches. The episodes of macropsia can occur as part of the aura in a migraine. These episodes are often brief, lasting only a few minutes. Adolescents who are deemed to have multiple distortions per episode, such as slow motion vision and macropsia, are even more likely to be people with migraine. The macropsia episodes associated with migraine are typically equivalent to the duration of the aura, which can range from moments to 15 minutes. Non-migrainous headaches are not known to be associated with episodic illusions. Even in the absence of a migraine, a fever or a hypnogogic state can provoke visual illusions, which one might claim to be macropsia. A person with macropsia may fail to see the connection between the migraine and the macropsia, since the conditions may not elicit symptoms at the same time. The pathophysiology of the condition is not fully understood, but the timing of some episodic occurrences with the headaches suggests that there is a connection between macropsia and the vasoconstrictive phase of a migraine. The differences in visual phenomena, such as macropsia with slow motion versus macropsia without slow motion, may result from different areas of the brain being affected by migraine.

Epilepsy
Macropsia may present itself as a symptom of both frontal lobe epilepsy and temporal lobe epilepsy, which may actually help in the diagnosis of those diseases. Children who experience nocturnal hallucinations accompanied by macropsia may seek medical care for panic attack disorders and instead are diagnosed with forms of epilepsy. Epilepsy patients may have no memory of the seizure, but can remember the hallucinations and aura which proceed the attack. Electroencephalography, or EEG imaging, can then be utilized while the patient experiences the episode. It may be subsequently concluded that the EEG is congruent with temporal or frontal lobe seizure. Anxiety and headaches accompany the episodes of visual distortion associated with epilepsy. While Valproic acid has been used to treat this type of seizure, anti-seizure medications appropriate for focal-onset seizures, like oxcarbazapine, have also been used successfully in the treatment of epilepsy-related macropsia.

Hypoglycaemia
Endogenous hypoglycaemia can result in number of visual disturbances and sometimes macropsia. This kind of hypoglycaemia is defined as having an abnormally low blood-sugar level due to anything other than the exogenous administration of insulin. Macropsia has been observed in experimental hypoglycaemia and in patients receiving insulin therapy.

Viruses
Patients with both Epstein-Barr virus and infectious mononucleosis have cited an increase in the sizes of perceived objects, coinciding with other symptoms of Alice in Wonderland Syndrome. Additionally, it has been observed that Epstein-Barr patients who cite hallucinations display abnormal MRI scans. The MRI may show swelling of the cerebral cortex, transient T2 prolongation, and transient lesions. Unlike in MRIs, no abnormalities have been reported in CT scans. It is thus recommended that an Epstein-Barr patient who cites visual hallucinations have an MRI scan. Macropsia may appear either before the onset, or after the resolution, of all clinical symptoms associated with the illness. The duration of the disturbances have been shown to range between two weeks and seven months. Almost all patients with macropsia due to infectious mononucleosis make full recoveries. Patients with Coxsackievirus B1 have reported numerous symptoms of Alice in Wonderland Syndrome, the most common of which being macropsia and micropsia.

Pathophysiology
Macropsia may be a result of optical magnification differences between the eyes, retinal receptor distribution, or the cortical processing of the sampled image. The current hypothesis for the occurrence of dysmetropsia is due to the stretching or compression of the retina leading to the displacement of receptors. Macropsia arises from a compressed receptor distribution leading to a larger perceived image size and conversely, micropsia results from stretching of the retina leading to a more sparse receptor distribution that gives a smaller perceived image size. In the case of macropsia, the greater density of photoreceptor cells leads to greater stimulation making the object seem larger. In some cases, the effects of macropsia have been shown to be field dependent, in that the degree of visual distortion is related to the visual field angle. Non-uniform stretching or compression of the receptor distribution could explain the field dependency of the macropsia. If the compression forces were closer to the fovea the resulting compression would cause a greater amount of macropsia at lower field angles with little effect at higher field angles where the receptor distribution is not as compressed. Alterations in receptor distribution can be the result of epiretinal membrane, neuroretina detachment and/or re-attachment, or retinoschisis. Macropsia caused by surgical re-attachment of macula-off rhegmatogenous retinal detachment is not symmetrical around the fovea, resulting in differences size changes in the horizontal and vertical meridians. Asymmetry has also been observed with retinoschisis, in which macropsia generally results in the vertical direction while micropsia presents in the horizontal direction.

Diagnosis
Macropsia is generally diagnosed once a patient complains of the characteristic symptoms, such as disproportionally large objects in their visual field. The Amsler Grid test can be used to diagnose macropsia, along with other visual maladies depending on the subjective disturbance reported by the patient after looking at the Amsler Grid. Outward bulging of the lines on an Amsler Grid is consistent with patients experiencing macropsisa. The New Aniseikonia Test (NAT) can quantify the degree of macropsia or micropsia independently in the vertical and horizontal meridians. The test consists of red and green semicircles on a black background with a white round fixation target. The size of the red semicircle is held constant while the green semicircle is varied in size in 1% increments. The patient wears a pair of red/green goggles so that one eye is tested at a time, and the patient attempts to determine when the semicircles are the same size. This is termed the reversal threshold and the size difference between the semicircles is reported as the degree of aniseikonia. A positive value indicates that the object was perceived bigger and thus corresponds to macropsia, and conversely a negative value indicates micropsia. The Aniseikonia Inspector contains an aniseikonia test based on the same principles as the NAT, but the test is run on a computer screen, it is based on a forced choice method, and it can measure the size difference as a function of the size of the objects </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Rolandic epilepsy and explain in detail? [/INST] Benign Rolandic epilepsy or benign childhood epilepsy with centrotemporal spikes (BCECTS) is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome (it starts around the age of 3–13 with a peak around 8–9 years and stops around age 14–18), hence the label benign. The seizures, sometimes referred to as sylvian seizures, start around the central sulcus of the brain (also called the centrotemporal area, located around the Rolandic fissure, after Luigi Rolando).

Signs and symptoms
The cardinal features of Rolandic epilepsy are infrequent, often single, focal seizures consisting of:
a. unilateral facial sensorimotor symptoms (30% of patients)
b. oropharyngolaryngeal manifestations (53% of patients)
c. speech arrest (40% of patients), and
d. hypersalivation (30% of patients)Hemifacial sensorimotor seizures are often entirely localised in the lower lip or spread to the ipsilateral hand. Motor manifestations are sudden, continuous or bursts of clonic contractions, usually lasting from a few seconds to a minute. Ipsilateral tonic deviation of the mouth is also common. Hemifacial sensory symptoms consist of unilateral numbness mainly in the corner of the mouth.
Hemifacial seizures are often associated with an inability to speak and hypersalivation:
The left side of my mouth felt numb and started jerking and pulling to the left, and I could not speak to say what was happening to me.
Negative myoclonus can be observed in some cases, as an interruption of tonic muscular activity
Oropharyngolaryngeal ictal manifestations are unilateral sensorimotor symptoms inside the mouth. Numbness, and more commonly paraesthesias (tingling, prickling, freezing), are usually diffuse on one side or, exceptionally, may be highly localised even to one tooth. Motor oropharyngolaryngeal symptoms produce strange sounds, such as death rattle, gargling, grunting and guttural sounds, and combinations:
In his sleep, he was making guttural noises, with his mouth pulled to the right, ‘as if he was chewing his tongue’. We heard her making strange noises ‘like roaring’ and found her unresponsive, head raised from the pillow, eyes wide open, rivers of saliva coming out of her mouth, rigid.
Arrest of speech is a form of anarthria. The child is unable to utter a single intelligible word and attempts to communicate with gestures.
My mouth opened and I could not speak. I wanted to say I cannot speak. At the same time, it was as if somebody was strangling me.
Hypersalivation, a prominent autonomic manifestation, is often associated with hemifacial seizures, oro-pharyngo-laryngeal symptoms and speech arrest. Hypersalivation is not just frothing:
Suddenly my mouth is full of saliva, it runs out like a river and I cannot speak.
Syncope-like epileptic seizures may occur, probably as a concurrent symptom of Panayiotopoulos syndrome:
She lies there, unconscious with no movements, no convulsions, like a wax work, no life.
Consciousness and recollection are fully retained in more than half (58%) of Rolandic seizures.
I felt that air was forced into my mouth, I could not speak and I could not close my mouth. I could understand well everything said to me. Other times I feel that there is food in my mouth and there is also a lot of salivation. I cannot speak.
In the remainder (42%), consciousness becomes impaired during the ictal progress and in one third there is no recollection of ictal events.
Progression to hemiconvulsions or generalised tonic-clonic seizures occurs in around half of children and hemiconvulsions may be followed by postictal Todds hemiparesis.
Duration and circadian distribution: Rolandic seizures are usually brief, lasting for 1–3 minutes. Three-quarters of seizures occur during nonrapid eye movement sleep, mainly at sleep onset or just before awakening.
Status epilepticus: Although rare, focal motor status or hemiconvulsive status epilepticus is more likely to occur than secondarily generalised convulsive status epilepticus, which is exceptional. Opercular status epilepticus usually occurs in children with atypical evolution or may be induced by carbamazepine or lamotrigine. This state lasts for hours to months and consists of ongoing unilateral or bilateral contractions of the mouth, tongue or eyelids, positive or negative subtle perioral or other myoclonus, dysarthria, speech arrest, difficulties in swallowing, buccofacial apraxia and hypersalivation. These are often associated with continuous spikes and waves on an EEG during NREM sleep.
Other seizure types: Despite prominent hypersalivation, focal seizures with primarily autonomic manifestations (autonomic seizures) are not considered part of the core clinical syndrome of Rolandic epilepsy.  However, some children may present with independent autonomic seizures or seizures with mixed Rolandic-autonomic manifestations including emesis as in Panayiotopoulos syndrome.Atypical forms:  Rolandic epilepsy may present with atypical manifestations such early age at onset, developmental delay or learning difficulties at inclusion, other seizure types, atypical EEG abnormalities.These children usually have normal intelligence and development. Learning can remain unimpaired while a child is afflicted with Rolandic epilepsy.

Cause
Benign epilepsy with centrotemporal spikes is thought to be a genetic disorder. An autosomal dominant inheritance with age dependency and variable penetrance has been reported, although not all studies support this theory. Linkage studies have pointed to a possible susceptibility region on chromosome 15q14, in the vicinity of the alpha-7 subunit of the acetylcholine receptor. Most studies show a slight male predominance. Because of the benign course and age-specific occurrence, it is thought to represent a hereditary impairment of brain maturation.An association with ELP4 has been identified.

Diagnosis
The diagnosis can be confirmed when the characteristic centrotemporal spikes are seen on electroencephalography (EEG). Typically, high-voltage spikes followed by slow waves are seen. Given the nocturnal activity, a sleep EEG can often be helpful. Technically, the label "benign" can only be confirmed if the childs development continues to be normal during follow-up </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Horizontal gaze palsy and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Meiges syndrome and explain in detail? [/INST] Meiges syndrome is a type of dystonia. It is also known as Brueghels syndrome and oral facial dystonia. It is actually a combination of two forms of dystonia, blepharospasm and oromandibular dystonia (OMD).
When OMD is combined with blepharospasm, it may be referred to as Meiges Syndrome named after Henri Meige, the French neurologist who first described the symptoms in detail in 1910. The symptoms usually begin between the ages of 30 and 70 years old and appear to be more common in women than in men (2:1 ratio). The combination of upper and lower dystonia is sometimes called cranial-cervical dystonia. The incidence is about one case in 20,000 people.

Presentation
The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle.  Some Meiges patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.The condition tends to affect women more frequently than men.

Symptoms
Oromandibular Symptoms

difficulty opening the mouth (trismus)
clenching or grinding of the teeth (bruxism)
spasms of jaw opening
sideways deviation or protrusion of the jaw
lip tightening and pursing
drawing back (retraction) of the corners of the mouth
deviation or protrusion of the tongue.
jaw pain
difficulties eating and drinking
difficulties speaking (dysarthria)Blepharospasm symptoms

the first symptom to appear is an increased rate of blinking
uncontrollable squinting/closing of eyes
light sensitivity (photophobia)
squinting/eyes closing during speech
uncontrollable eyes closing shut (rare instances completely causing blindness)In addition, in some patients, the dystonic spasms may sometimes be provoked by certain activities, such as talking, chewing, or biting. Particular activities or sensory tricks may sometimes temporarily alleviate OMD symptoms, including chewing gum, talking, placing a toothpick in the mouth, lightly touching the lips or chin, or applying pressure beneath the chin.

Diagnosis
Meiges is commonly misdiagnosed and most doctors will not be familiar with this condition due to its rare incidence. Usually, a neurologist specializing in psychomotor disorders can detect Meiges. There are currently no technological diagnostic tools to detect Meiges, as it cannot be identified using blood chemistry analysis or radiological imaging, such as MRI or CT scans. A patient presenting with signs of OMD alone may be misdiagnosed with TMJD.Patients with idiopathic Meiges syndrome do not quickly respond to anticholinergic drug treatments, a diagnostic sign that can help differentiate it from acute dystonia, which does respond to anticholinergic drugs.

Upper and lower dystonia types
The Greek word blepharon means "eyelid". Spasm means "uncontrolled muscle contraction". The term blepharospasm [blef-a-ro-spaz-m] can be applied to any abnormal blinking or eyelid tic or twitch resulting from any cause, ranging from dry eyes to Tourettes syndrome to tardive dyskinesia. The blepharospasm referred to here is officially called benign essential blepharospasm (BEB) to distinguish it from the less serious secondary blinking disorders. "Benign" indicates the condition is not life-threatening, and "essential" is a medical term meaning "of unknown cause". It is both a cranial and a focal dystonia. Cranial refers to the head and focal indicates confinement to one part. The word dystonia describes abnormal involuntary sustained muscle contractions and spasms. Patients with blepharospasm have normal eyes. The visual disturbance is due solely to the forced closure of the eyelids.Oromandibular dystonia (OMD) is a form of focal dystonia that affects varying areas of the head and neck including the lower face, jaw, tongue and larynx.  The spasms may cause the mouth to pull open, shut tight, or move repetitively.  Speech and swallowing may be distorted.  It is often associated with dystonia of the cervical muscles (Spasmodic Torticollis), eyelids (Blepharospasm), or larynx (Spasmodic Dysphonia).In patients with OMD, involuntary contractions may involve the muscles used for chewing (masticatory muscles). These may include the thick muscle in the cheek that closes the jaw (masseter muscle) and the broad muscle that draws back the lower jaw and closes the mouth (temporalis muscle). Some patients may also experience involuntary contractions of the wide muscle at the side of the neck (platysmal muscle). This muscle draws down the corner of the mouth and lower lip or other muscle groups.

Treatment
In some cases Meiges syndrome can be reversed when it is caused by medication. Botulinum toxin injections can be helpful for the blepharospasm and for masseter spasm.

See also
Mogigraphia

References

Paulson, George W </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mastitis and explain in detail? [/INST] Mastitis is inflammation of the breast or udder, usually associated with breastfeeding. Symptoms typically include local pain and redness. There is often an associated fever and general soreness. Onset is typically fairly rapid and usually occurs within the first few months of delivery. Complications can include abscess formation.Risk factors include poor latch, cracked nipples, use of a breast pump, and weaning. The bacteria most commonly involved are Staphylococcus and Streptococci. Diagnosis is typically based on symptoms. Ultrasound may be useful for detecting a potential abscess.Prevention is by proper breastfeeding techniques. When infection is present, antibiotics such as cephalexin may be recommended. Breastfeeding should typically be continued, as emptying the breast is important for healing. Tentative evidence supports benefits from probiotics. About 10% of breastfeeding women are affected.

Types
When it occurs in breastfeeding mothers, it is known as puerperal mastitis, lactation mastitis, or lactational mastitis. When it occurs in non breastfeeding women it is known as non-puerperal or nonlactational. Mastitis can, in rare cases, occur in men. Inflammatory breast cancer has symptoms very similar to mastitis and must be ruled out.
The symptoms are similar for puerperal and nonpuerperal mastitis but predisposing factors and treatment can be very different.

Pregnancy related
Puerperal mastitis is the inflammation of the breast in connection with pregnancy, breastfeeding or weaning. Since one of the most prominent symptoms is tension and engorgement of the breast, it is thought to be caused by blocked milk ducts or milk excess. It is relatively common; estimates range depending on methodology between 5–33%. However, only about 0.4–0.5% of breastfeeding mothers develop an abscess.Some predisposing factors are known but their predictive value is minimal. It appears that proper breastfeeding technique, frequent breastfeeding and avoidance of stress are the most important factors that can be influenced.
Light cases of mastitis are often called breast engorgement; the distinction is overlapping and possibly arbitrary or subject to regional variations.

Non pregnancy related
The term nonpuerperal mastitis describes inflammatory lesions of the breast occurring unrelated to pregnancy and breastfeeding. This article includes description of mastitis as well as various kinds of mammary abscesses. Skin related conditions like dermatitis and foliculitis are a separate entity.
Names for non-puerperal mastitis are not used very consistently and include mastitis, subareolar abscess, duct ectasia, periductal inflammation, Zuskas disease and others.
Periductal mastitis is a form of nonlactational mastitis, and is characterized by inflammation of the subareolar ducts. Although the cause of periductal mastitis is currently unknown, it is predicted that smoking may be related. This condition is mainly seen in young women but can also be seen in men.

Signs and symptoms
Lactation mastitis usually affects only one breast and the symptoms can develop quickly. It develops into three stages, from the initial stage, the pus formation stage, to the restoration stage. The signs and symptoms usually appear suddenly and they include:

Breast tenderness or warmth to the touch
General malaise or feeling ill
Swelling of the breast
Pain or a burning sensation continuously or while breast-feeding
Skin redness, often in a wedge-shaped pattern
Fever of 101 F (38.3 C) or greater
The affected breast can then start to appear lumpy and red.Some women may also experience flu-like symptoms such as:

Aches
Shivering and chills
Feeling anxious or stressed
FatigueContact should be made with a health care provider with special breastfeeding competence as soon as the patient recognizes the combination of signs and symptoms. Most of the women first experience the flu-like symptoms and just after they may notice a sore red area on the breast. Also, women should seek medical care if they notice any abnormal discharge from the nipples, if  breast pain is making it difficult to function each day, or they have prolonged, unexplained breast pain.

Breast abscess
A breast abscess is a collection of pus that develops in the breast with various causes. During lactation, breast abscess develops only rarely, most sources cite about 0.4–0.5% of breastfeeding women. Known risk factors are age over 30, primiparous and late delivery. No correlation was found with smoking status; however, this may be in part because far fewer smoking women choose to breastfeed. Antibiotics were not shown effective in prevention of lactation abscess but are useful to treat a secondary infection (see the section on the treatment of breast abscess in this article).
Keratinizing squamous metaplasia of lactiferous ducts may play a similar role in the pathogenesis of nonpuerperal subareolar abscess.

Causes
Since the 1980s mastitis has often been divided into non-infectious and infectious sub-groups. However, recent research  suggests that it may not be feasible to make divisions in this way. It has been shown that types and amounts of potentially pathogenic bacteria in breast milk are not correlated to the severity of symptoms. Moreover, although only 15% of women with mastitis in Kvist et al.s study were given antibiotics, all recovered and few had recurring symptoms. Many healthy breastfeeding women wishing to donate breast milk have potentially pathogenic bacteria in their milk but have no symptoms of mastitis.

Risk factors
Mastitis typically develops when the milk is not properly removed from the breast. Milk stasis can lead to the milk ducts in the breasts becoming blocked, as the breast milk is not being properly and regularly expressed. It has also been suggested that blocked milk ducts can occur as a result of pressure on the breast, such as tight-fitting clothing or an over-restrictive bra, although there is sparse evidence for this supposition.
Mastitis may  occur when the baby is not appropriately attached to the breast while feeding, when the baby has infrequent feeds or has problems suckling the milk out of the breast.
The presence of cracks or sores on the nipples increases the likelihood of infection. Tight clothing or ill-fitting bras may also cause problems as they compress the breasts.  There is a possibility that infants carrying infectious pathogens in their noses can infect their mothers; the clinical significance of this finding is still unknown.
Mastitis and breast abscesses can also be caused by direct trauma to the breast. Such injury can occur for example during sports activities or due to seat belt injury.
Mastitis can also develop due to contamination of a breast implant or any other foreign body, for example after nipple piercing. In such cases, the removal of the foreign body is indicated.Women who are breastfeeding are at risk for developing mastitis especially if they have sore or cracked nipples or have had mastitis before while breastfeeding another baby. Also, the chances of getting mastitis increases if women use only one position to breastfeed or wear a tight-fitting bra, which may restrict milk flow  Difficulties in getting a nursing infant to latch on to the breast can also increase the risk for mastitis.Women with diabetes, chronic illness, AIDS, or an impaired immune system may be more susceptible to the development of mastitis.

Infection
Some women (approximately 15%) will require antibiotic treatment for infection which is usually caused by bacteria from the skin or the babys mouth entering the milk ducts through skin lesions of the nipple or through the opening of the nipple. Infection is usually caused by Staphylococcus aureus. Infectious pathogens commonly associated with mastitis are Staphylococcus aureus, Streptococcus spp. and Gram-negative bacilli such as Escherichia coli. Salmonella spp., mycobacteria, and fungi such as Candida and Cryptococcus have been identified in rare instances.Recent research suggests that infectious pathogens play a much smaller role in the pathogenesis than was commonly assumed only a few years ago. Most detected pathogens are very common species that are natural part of the breast fauna and simple detection of their presence is not sufficient to prove a causative role. Furthermore, there are indications that treatment with antibiotics may have minimal impact, and over-all there is insufficient evidence to confirm or refute the effectiveness of antibiotic therapy for treating lactational mastitis.

Diagnosis
The diagnosis of mastitis and breast abscess can usually be made based on a physical examination. The doctor will also take into account the signs and symptoms of the condition.
However, if the doctor is not sure whether the mass is an abscess or a tumor, a breast ultrasound may be performed. The ultrasound provides a clear image of the breast tissue and may be helpful in distinguishing between simple mastitis and abscess or in diagnosing an abscess deep in the breast. The test consists of placing an ultrasound probe over the breast.
In cases of infectious mastitis, cultures may be needed in order to determine what type of organism is causing the infection. Cultures are helpful in deciding the specific type of antibiotics that will be used in curing the disease. These cultures may be taken either from the breast milk or of the material aspirated from an abscess.
Mammograms or breast biopsies are normally performed on women who do not respond to treatment or on non-breastfeeding women. This type of tests is sometimes ordered to exclude the possibility of a rare type of breast cancer which causes symptoms similar to those of mastitis.

Differential diagnosis
Breast cancer may coincide with or mimic symptoms of mastitis. Only full resolution of symptoms and careful examination are sufficient to exclude the diagnosis of breast cancer.
Lifetime risk for breast cancer is significantly reduced for women who were pregnant and breastfeeding. Mastitis episodes do not appear to influence lifetime risk of breast cancer.
Mastitis does however cause great difficulties in diagnosis of breast cancer and delayed diagnosis and treatment can result in worse outcome.
Breast cancer may coincide with mastitis or develop shortly afterwards. All suspicious symptoms that do not completely disappear within 5 weeks must be investigated.
Breast cancer incidence during pregnancy and lactation is assumed to be the same as in controls. Course and prognosis are also very similar to age matched controls. However diagnosis during lactation is particularly problematic, often leading to delayed diagnosis and treatment.
Some data suggest that noninflammatory breast cancer incidence is increased within a year following episodes of nonpuerperal mastitis and special care is required for follow-up cancer prevention screening. So far only data from short term observation is available and total risk increase can not be judged. Because of the very short time between presentation of mastitis and breast cancer in this study it is considered very unlikely that the inflammation had any substantial role in carcinogenesis, rather it would appear that some precancerous lesions may increase the risk of inflammation (hyperplasia causing duct obstruction, hypersensitivity to cytokines or hormones) or the lesions may have common predisposing factors.
A very serious type of breast cancer called inflammatory breast cancer presents with similar symptoms as mastitis (both puerperal and nonpuerperal). It is the most aggressive type of breast cancer with the highest mortality rate. The inflammatory phenotype of IBC is thought to be mostly caused by invasion and blocking of dermal lymphatics, however it was recently shown that NF-κB target genes activation may significantly contribute to the inflammatory phenotype. Case reports show that inflammatory breast cancer symptoms can flare up following injury or inflammation making it even more likely to be mistaken for mastitis. Symptoms are also known to partially respond to progesterone and antibiotics, reaction to other common medications can not be ruled out at this point.

Treatment
In lactation mastitis, frequent emptying of both breasts by breastfeeding is essential. Also essential is adequate fluid supply for the mother and baby.
For breastfeeding women with light mastitis, massage and application of heat prior to feeding can help as this may aid unblocking the ducts. However, in more severe cases of mastitis heat or massage could make the symptoms worse and cold compresses are better suited to contain the inflammation.
Nonpuerperal mastitis is treated by medication and possibly aspiration or drainage (see in particular treatment of subareolar abscess and treatment of granulomatous mastitis). According to a BMJ best practice report, antibiotics are generally to be used in all nonpuerperal mastitis cases, with replacement of the antibiotics by an antifungal agent such as fluconazole in cases of deep fungal infections, and corticosteroids are to be used in case of granulomatous mastitis (with differential diagnosis to tuberculosis infection of the breast).In idiopathic granulomatous mastitis, successful treatment includes invasive surgical procedures or less invasive treatment with steroid medications.

Antibiotics
In lactational mastitis, antibiotics are not needed in the overwhelming majority of cases and should be used only for bacterial infections. For people with nonsevere infections, dicloxacillin or cephalexin are recommended. For people with severe infections, vancomycin is recommended. The length of antibiotic treatment ranges anywhere from 5–14 days. The effects of antibiotics has not been well studied as of 2013.

Breast abscess
An abscess (or suspected abscess) in the breast may be treated by ultrasound-guided fine-needle aspiration (percutaneous aspiration) or by surgical incision and drainage; each of these approaches is performed under antibiotic coverage. In case of puerperal breast abscess, breastfeeding from the affected breast should be continued where possible.For small breast abscesses, ultrasound-guided fine needle aspiration such as to completely drain the abscess is widely recognized as a preferred initial management.One recommended treatment includes antibiotics, ultrasound evaluation and, if fluid is present, ultrasound-guided fine needle aspiration of the abscess with an 18 gauge needle, under saline lavage until clear. The exudate is then sent for microbiological analysis for identification of the pathogen and determination of its antibiotic sensitivity profile, which may in turn give an indication for changing the antibiotics. At follow-up, a mammography is performed if the condition has resolved; otherwise the ultrasound-guided fine-needle aspiration with lavage and microbiological analysis is repeated. If three to five aspirations still do not resolve the condition, percutaneous drainage in combination with placement of an indwelling catheter is indicated, and only if several attempts at ultrasound-guided drainage fail, surgical resection of the inflamed lactiferous ducts (preferably performed after the acute episode is over). It is noted, however, that even the excision of the affected ducts does not necessarily prevent recurrence.Nonpuerperal breast abscesses have a higher rate of recurrence compared to puerperal breast abscesses. There is a high statistical correlation of nonpuerperal breast abscess with diabetes mellitus (DM). On this basis, it has recently been suggested that diabetes screening should be performed on patients with such abscess.Although there are a number of recommendations regarding the treatment of breast abscesses, a 2015 review found insufficient evidence of whether needle aspiration is comparable to incision and drainage, or whether antibiotics should generally be given to women undergoing incision and drainage.

Prognosis
Temperature and severity of symptoms at presentation do not predict outcome; women with sore or damaged nipples may need special attention.

Epidemiology
Mastitis is quite common among breastfeeding women. The WHO estimates that although incidences vary between 2.6% and 33%, the prevalence globally is approximately 10% of breastfeeding women. Most mothers who develop mastitis  usually do so within the first few weeks after delivery. Most breast infections occur within the first or second month after delivery or at the time of weaning </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Congenital trigger thumb and explain in detail? [/INST] Congenital trigger thumb is a trigger thumb in infants and young children. Triggering, clicking or snapping is observed by flexion or extension of the interphalangeal joint (IPJ). In the furthest stage, no extension is possible and there is a fixed flexion deformity of the thumb in the IPJ. Cause, natural history, prognosis and recommended treatment are controversial.

Signs and symptoms
Besides the clicking, snapping or triggering, a characteristic Notta nodule is commonly found on the palmar side at the metacarpophalangeal (MCP) joint. This nodule can be found by palpation. Children can also present a thumb which they cannot extend actively due to entrapment of the nodule to the A1 pulley. Some may even present with a fixed flexion deformity of the IPJ where no extension is possible.

Cause
It is unclear whether the cause of the trigger thumb is congenital or acquired. The occurrence of bilateral incidence and trigger thumbs in both children of twins are an indication for a congenital cause. Trigger thumb in children is also associated with trisomy of chromosome 13. For these reasons it was assumed that trigger thumbs in children are to be of congenital cause. However, more and more evidence which point towards an acquired cause have been found in recent studies. Therefore, the name pediatric trigger thumb is also widely used (and currently preferred by some) for the same disorder.

Diagnosis
Diagnosis of a trigger thumb is solely made by these clinical observations and further classified into four stages:

Treatment
There are several types of treatment for congenital trigger thumb, conservative and surgical.

Conservative
The conservative treatment consists of observation in time. Studies show that the trigger thumb spontaneously resolves in 49 months. According to Leung et al., trigger thumbs in infants resolve spontaneously in 63% of the cases. No residual deformities were found and there is no recurrence once resolved. Residual deformity is defined as persistent flexion deformities of the thumb and radial deviation at the IPJ. Extension exercises and splinting can be added to the observation. These two elements have favourable results in improvement in flexion impairment of the thumb. However, compared to observation, the benefit of merely extension exercises and splinting are still unclear.It has been recommended to attempt conservative treatment first, before attempting surgical treatment.

Surgical
Surgical treatment should be considered when the patient has a trigger thumb bilaterally and when the patient has a severe trigger thumb. Severe is defined as when the thumb is locked so that the thumb cannot be flexed or extended either passively or actively. Surgical treatment should also be considered when observation and/or splint therapy has not achieved sufficient results after 49 months. Unlike the surgical treatment given for adults, which is unambiguously a surgical release of the A1 pulley of the thumb, the optimum surgical treatment for infants has not yet been discerned. In case of infants, research has shown that only in 15% of the cases A1 pulley release alone is sufficient. In most of the cases there was an additional annular pulley structure distal to the A1 to be released resolving the triggering: the so-called Av pulley or variable pulley. Therefore, infants and adults need to be treated differently as the main problem is different.

Open vs. percutaneous
There are two types of surgery: open surgery which is mentioned above and percutaneous surgery. Unlike open surgery percutaneous surgery is done without exposing the anatomical structures beneath the skin. Research has shown that percutaneous surgery is a good alternative to open surgery. Percutaneous surgery is done with a needle that is inserted in the flexor sheath at the level of the A1 pulley. Before the needle insertion the thumb is placed in extension, whereas when the needle is already inserted the thumb will be put into semi-flexion, so that the needle can be moved and the palmar skin is movable </s>