During a period of 13 years (1980–1993) for which admissions to the Kfar Shaul Mental Health Centre in Jerusalem were analysed, it was reported that 1,200 tourists with severe, Jerusalem-themed mental problems were referred to this clinic. Of these, 470 were admitted to hospital. On average, 100 such tourists have been seen annually, 40 of them requiring admission to hospital. About three and a half million tourists visit Jerusalem each year. Kalian and Witztum note that as a proportion of the total numbers of tourists visiting the city, this is not significantly different from any other city.

Jerusalem syndrome is a group of mental phenomena involving the presence of either religiously themed obsessive ideas, delusions or other psychosis-like experiences that are triggered by a visit to the city of Jerusalem. It is not endemic to one single religion or denomination but has affected Jews, Christians, and Muslims of many different backgrounds.

The best known, although not the most prevalent, manifestation of Jerusalem syndrome is the phenomenon whereby a person who seems previously balanced and devoid of any signs of psychopathology becomes psychotic after arriving in Jerusalem. The psychosis is characterised by an intense religious theme and typically resolves to full recovery after a few weeks or after being removed from the area. The religious focus of Jerusalem syndrome distinguishes it from other phenomena, such as Stendhal syndrome in Florence or Paris syndrome for Japanese tourists.

In a 2000 article in the "British Journal of Psychiatry", Bar-El et al. claim to have identified and described a specific syndrome which emerges in tourists with no previous psychiatric history. However, this claim has been disputed by M. Kalian and E. Witztum. Kalian and Witztum stressed that nearly all of the tourists who demonstrated the described behaviours were mentally ill prior to their arrival in Jerusalem. They further noted that, of the small proportion of tourists alleged to have exhibited spontaneous psychosis after arrival in Jerusalem, Bar-El et al. had presented no evidence that the tourists had been well prior to their arrival in the city. Jerusalem syndrome is not listed or mentioned in the DSM nor in the ICD.

Paris syndrome (, , "Pari shōkōgun") is a transient mental disorder exhibited by some individuals when visiting or going on vacation to Paris, as a result of extreme shock derived from their discovery that Paris is not what they had expected it to be. The syndrome is characterized by a number of psychiatric symptoms such as acute delusional states, hallucinations, feelings of persecution (perceptions of being a victim of prejudice, aggression, or hostility from others), derealization, depersonalization, anxiety, and also psychosomatic manifestations such as dizziness, tachycardia, sweating, and others, such as vomiting. Similar syndromes include Jerusalem syndrome and Stendhal syndrome. The condition is commonly viewed as a severe form of culture shock. It is particularly noted among Japanese travelers.

Professor Hiroaki Ota, a Japanese psychiatrist working in France, is credited as the first person to diagnose the condition in 1986. However, later work by Youcef Mahmoudia, physician with the hospital Hôtel-Dieu de Paris, indicates that Paris syndrome is "a manifestation of psychopathology related to the voyage, rather than a syndrome of the traveller." He theorized that the excitement resulting from visiting Paris causes the heart to accelerate, causing giddiness and shortness of breath, which results in hallucinations in the manner similar to the Stendhal syndrome described by Italian psychiatrist Graziella Magherini in her book "La sindrome di Stendhal".

A syndrome is a set of medical signs and symptoms occurring together, constitutes a particular disease or disorder. The word derives from the Greek σύνδρομον, meaning "concurrence". In some instances, a syndrome is so closely linked with a pathogenesis or cause that the words "syndrome", "disease", and "disorder" end up being used interchangeably for them. This is especially true of inherited syndromes. For example, Down syndrome, Wolf–Hirschhorn syndrome, and Andersen syndrome are disorders with known pathogeneses, so each is more than just a set of signs and symptoms, despite the "syndrome" nomenclature. In other instances, a syndrome is not specific to only one disease. For example, toxic shock syndrome can be caused by various toxins; premotor syndrome can be caused by various brain lesions; and premenstrual syndrome is not a disease but simply a set of symptoms.

If an underlying genetic cause is suspected but not known, a condition may be referred to as a genetic association (often just "association" in context). By definition, an association indicates that the collection of signs and symptoms occurs in combination more frequently than would be likely by chance alone.

Syndromes are often named after the physician or group of physicians that discovered them or initially described the full clinical picture. Such eponymous syndrome names are examples of medical eponyms. Recently, there has been a shift towards naming conditions descriptively (by symptoms or underlying cause) rather than eponymously, but the eponymous syndrome names often persist in common usage.

In medicine a broad definition of syndrome is used, which describes a collection of symptoms and findings without necessarily tying them to a single identifiable pathogenesis. The more specific definition employed in medical genetics describes a subset of all medical syndromes.

As the syndrome is due to a chromosomal non-disjunction event, the recurrence risk is not high compared to the general population. There has been no evidence found that indicates non-disjunction occurs more often in a particular family.

Anti-Arabism, Anti-Arab sentiment or Arabophobia is opposition to, or dislike, fear, hatred, and advocacy of genocide of Arab people.

Historically, anti-Arab prejudice has been suggested by such events as the reconquest of the Iberian Peninsula, the condemnation of Arabs in Spain by the Spanish Inquisition, the Zanzibar Revolution in 1964, and the 2005 Cronulla riots in Australia. In the current era, racial prejudice against Arabs is apparent in many countries including Iran, Poland, France, Australia, Israel, and the United States (including Hollywood). Various advocacy organizations have been formed to protect the civil rights of Arab citizens in the United States, such as the American-Arab Anti-Discrimination Committee (ADC) and the Council on American-Islamic Relations (CAIR).

Xenophobia is the fear and distrust of that which is perceived to be foreign or strange. Xenophobia can manifest itself in many ways involving the relations and perceptions of an ingroup towards an outgroup, including a fear of losing identity, suspicion of its activities, aggression, and desire to eliminate its presence to secure a presumed purity. Xenophobia is a political term and not a recognized medical phobia.

Xenophobia can also be exhibited in the form of an "uncritical exaltation of another culture" in which a culture is ascribed "an unreal, stereotyped and exotic quality". The terms xenophobia and racism are sometimes confused and used interchangeably because people who share a national origin may also belong to the same race. Due to this, xenophobia is usually distinguished by opposition to foreign culture.

After the first discovery and description of Marshall–Smith syndrome in 1971, research to this rare syndrome has been carried out.

- Adam, M., Hennekam, R.C.M., Butler, M.G., Raf, M., Keppen, L., Bull, M., Clericuzio, C., Burke, L., Guttacher, A., Ormond, K., & Hoyme, H.E. (2002). Marshall–Smith syndrome: An osteochondrodysplasia with connective tissue abnormalities. 23rd Annual David W. Smith Workshop on Malformations and Morphogenesis, August 7, Clemson, SC.

- Adam MP, Hennekam RC, Keppen LD, Bull MJ, Clericuzio CL, Burke LW, Guttmacher AE, Ormond KE and Hoyme HE: Marshall-Smith Syndrome: Natural history and evidence of an osteochondrodysplasia with connective tissue abnormalities. American Journal of Medical Genetics 137A:117–124, 2005.

- Baldellou Vazquez A, Ruiz-Echarri Zelaya MP, Loris Pablo C, Ferr#{225}ndez Longas A, Tamparillas Salvador M. El sIndrome de Marshall-Smith: a prop#{243}sito de una observad#{243}n personal. An Esp Pediatr 1983; 18:45-50.

- Butler, M.G. (2003). Marshall–Smith syndrome. In: The NORD Guide to Rare Disorders. (pp219–220) Lippincott, Williams & Wilkins, Philadelphia, PA.

- Charon A, Gillerot T, Van Maldergem L, Van Schaftingen MH, de Bont B, Koulischer L. The Marshall–Smith syndrome. Eur J Pediatr 1990; 150: 54-5.

- Dernedde, G., Pendeville, P., Veyckemans, F., Verellen, G. & Gillerot, Y. (1998). Anaesthetic management of a child with Marshall–Smith syndrome. Canadian Journal of Anesthesia. 45 (7): 660. Anaesthetic management of a child with Marshall-Smith syndrome

- Diab, M., Raff, M., Gunther, D.F. (2002). Osseous fragility in Marshall–Smith syndrome. Clinical Report: Osseous fragility in Marshall-Smith syndrome

- Ehresmann, T., Gillessen-Kaesbach G., Koenig R. (2005). Late diagnosis of Marshall Smith Syndrome (MSS). In: Medgen 17.

- Hassan M, Sutton T, Mage K, LimalJM, Rappaport R. The syndrome of accelerated bone maturation in the newborn infant with dysmorphism and congenital malformations: (the so-called Marshall–Smith syndrome). Pediatr Radiol 1976; 5:53-57.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. Western Society for Pediatric Research, Carmel, California, February, 1987. Clin Res 35:68A, 1987.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. David W. Smith Morphogenesis and Malformations Workshop. Greenville, SC, August, 1987. Proceedings of the Greenwood Genetics Center 7:152, 1988.

- Hoyme HE, Byers PH, Guttmacher AE: Marshall–Smith syndrome: Further evidence of an osteochondrodysplasia in long-term survivors. David W. Smith Morphogenesis and Malformations Workshop, Winston-Salem, NC, August, 1992. Proceedings of the Greenwood Genetic Center 12:70, 1993.

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- Tzu-Jou Wang (2002). Marshall–Smith syndrome in a Taiwanese patient with T-cell immunodeficiency. Am J Med Genet Part A;112 (1):107-108.

In mild cases, individuals with XXXY syndrome may lead a relatively good life. These individuals may face difficulties in communicating with others due to their language-based deficits. These deficits may make forming bonds with others difficult, but fulfilling relationships with others are still achievable. Those with higher scores in adaptive functioning are likely to have higher quality of life because they can be independent.

Williams syndrome is a microdeletion syndrome caused by the spontaneous deletion of genetic material from the region q11.23 of one member of the pair of chromosome 7, so that the person is hemizygous for those genes. The deleted region includes more than 25 genes, and researchers believe that being hemizygous for these genes probably contributes to the characteristic features of this syndrome. "CLIP2", "ELN", "GTF2I", "GTF2IRD1", and "LIMK1" are among the genes that are typically deleted from one chromosome in people with Williams syndrome. Researchers have found this hemizygosity for the "ELN" gene, which codes for the protein elastin, is associated with the connective-tissue abnormalities and cardiovascular disease (specifically supravalvular aortic stenosis and supravalvular pulmonary stenosis) found in many people with this syndrome. The insufficient supply of elastin may also be the cause of full cheeks, harsh or hoarse voice, hernias and bladder diverticula often found in those with Williams syndrome. Studies suggest that hemizygosity in "LIMK1", "GTF2I", "GTF2IRD1", and perhaps other genes may help explain the characteristic difficulties with visual–spatial tasks. Additionally, there is evidence that the hemizygosity in several of these genes, including "CLIP2", may contribute to the unique behavioral characteristics, learning disabilities, and other cognitive difficulties seen in Williams syndrome.

Roberts syndrome is an extremely rare condition that only affects about 150 reported individuals. Although there have been only about 150 reported cases, the affected group is quite diverse and spread worldwide. Parental consanguinity (parents are closely related) is common with this genetic disorder. The frequency of Roberts syndrome carriers is unknown.

Marshall–Smith syndrome is not to be confused with:

- Marshall syndrome (aka.Periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA syndrome, see also: Periodic fever syndrome)

- Sotos (like) syndrome

- Weaver-Smith syndrome (WSS)

Familial dysautonomia is seen almost exclusively in Ashkenazi Jews and is inherited in an autosomal recessive fashion. Both parents must be carriers in order for a child to be affected. The carrier frequency in Jewish individuals of Eastern European (Ashkenazi) ancestry is about 1/30, while the carrier frequency in non-Jewish individuals is unknown. If both parents are carriers, there is a one in four, or 25%, chance with each pregnancy for an affected child. Genetic counseling and genetic testing is recommended for families who may be carriers of familial dysautonomia.

Worldwide, there have been approximately 600 diagnoses recorded since discovery of the disease, with approximately 350 of them still living.

More than 80% of children with Patau syndrome die within the first year of life. Children with the mosaic variation are usually affected to a lesser extent. In a retrospective Canadian study of 174 children with trisomy 13, median survival time was 12.5 days. One and ten year survival was 19.8% and 12.9% respectively.

The greatest risk factor for developing leprosy is contact with another case of leprosy. Contacts of people with leprosy are five to eight times more likely to develop leprosy than members of the general population. Leprosy also occurs more commonly among those living in poverty.

Other risk factors are poorly understood. However, conditions that reduce immune function, such as malnutrition, other illnesses, or host genetic differences, may increase the risk of developing leprosy. Despite this, infection with HIV does not appear to increase the risk of developing leprosy.

Those affected were born prematurely, and suffered from feeding difficulties and developmental delays. They presented with progressive kidney disease and primary pulmonary hypertension, and ultimately died.

It is not possible to make a generalised prognosis for development due to the variability of causes, as mentioned above, the differing types of symptoms and cause. Each case must be considered individually.

The prognosis for children with idiopathic West syndrome are mostly more positive than for those with the cryptogenic or symptomatic forms. Idiopathic cases are less likely to show signs of developmental problems before the attacks begin, the attacks can often be treated more easily and effectively and there is a lower relapse rate. Children with this form of the syndrome are less likely to go on to develop other forms of epilepsy; around two in every five children develop at the same rate as healthy children.

In other cases, however, treatment of West syndrome is relatively difficult and the results of therapy often dissatisfying; for children with symptomatic and cryptogenic West syndrome, the prognosis is generally not positive, especially when they prove resistant to therapy.

Statistically, 5 out of every 100 children with West syndrome do not survive beyond five years of age, in some cases due to the cause of the syndrome, in others for reasons related to their medication. Only less than half of all children can become entirely free from attacks with the help of medication. Statistics show that treatment produces a satisfactory result in around three out of ten cases, with only one in every 25 children's cognitive and motoric development developing more or less normally.

A large proportion (up to 90%) of children suffer severe physical and cognitive impairments, even when treatment for the attacks is successful. This is not usually because of the epileptic fits, but rather because of the causes behind them (cerebral anomalies or their location or degree of severity). Severe, frequent attacks can (further) damage the brain.

Permanent damage often associated with West syndrome in the literature include cognitive disabilities, learning difficulties and behavioural problems, cerebral palsy (up to 5 out of 10 children), psychological disorders and often autism (in around 3 out of 10 children). Once more, the cause of each individual case of West syndrome must be considered when debating cause and effect.

As many as 6 out of 10 children with West syndrome suffer from epilepsy later in life. Sometimes West syndrome turns into a focal or other generalised epilepsy. Around half of all children develop Lennox-Gastaut syndrome.

Williams syndrome has historically been estimated to occur in roughly 1 in every 20,000 live births. However, more recent epidemiological studies have placed the occurrence rate at closer to 1 in every 7,500 live births, a significantly larger prevalence. As an increasing body of evidence suggests that Williams syndrome is more common than originally noted (approximately 6% of all genetic cases of developmental disability), researchers have begun to theorize past under-diagnosis of the syndrome. One theorized reason for the increase in epidemiological estimates is that there exists a substantial minority of individuals with the genetic markers of Williams syndrome who lack the characteristic facial features or the diminished IQ considered to be diagnostic of the syndrome, who often are not immediately recognized as people with the syndrome.

West syndrome appears in 1% to 5% of infants with Down syndrome. This form of epilepsy is relatively difficult to treat in children who do not have the chromosomal abnormalities involved in Down syndrome. However, in children with Down syndrome, the syndrome is often far more mild, and the children often react better to medication. The German Down Syndrom InfoCenter noted in 2003 that what was normally a serious epilepsy was in such cases often a relatively benign one.

EEG records for children with Down syndrome are often more symmetrical with fewer unusual findings. Although not all children can become entirely free from attacks with medication, children with Down syndrome are less likely to go on to develop Lennox-Gastaut syndrome or other forms of epilepsy than those without additional hereditary material on the 21st chromosome. The reason why it is easier to treat children with Down syndrome is not known.

If, however, a child with Down syndrome has seizures that are difficult to control, the child should be accessed for autistic spectrum disorder.

HUPRA syndrome is a rare syndrome that was first described in 2010 in two infants of Palestinian origin from the same village in the Jerusalem area. One of the two infants' parents were related. It was later described in a third infant from the same village, whose parents were not related.

The acronym stands for Hyperuricemia, Pulmonary hypertension, Renal failure in infancy and Alkalosis. And it's due to mutations in the mitochondrial SARS enzyme. It's an autosomal recessive disease, that has a prevalence of less than one in a million. One in fifteen of the village's inhabitants were found to carry the genetic mutation.

Documented cases of Reye syndrome in adults are rare. The recovery of adults with the syndrome is generally complete, with liver and brain function returning to normal within two weeks of onset. In children, however, mild to severe permanent brain damage is possible, especially in infants. Over thirty percent of the cases reported in the United States from 1981 through 1997 resulted in fatality.

Typically, females and older patients with organic brain changes are more likely to develop Pisa syndrome. Organic brain changes are physical changes in the brain which lead to neurological dysfunction, including dementia and frontal lobe syndrome. This includes the presence of neurodegenerative illnesses such as Alzheimer's Disease and Parkinson's Disease.

Reye syndrome occurs almost exclusively in children. While a few adult cases have been reported over the years, these cases do not typically show permanent neural or liver damage. Unlike in the UK, the surveillance for Reye syndrome in the US is focused on patients under 18 years of age.

In 1980, after the CDC began cautioning physicians and parents about the association between Reye syndrome and the use of salicylates in children with chickenpox or virus-like illnesses, the incidence of Reye syndrome in the United States began to decline. However, the decline began prior to the FDA's issue of warning labels on aspirin in 1986. In the United States between 1980 and 1997, the number of reported cases of Reye syndrome decreased from 555 cases in 1980 to about 2 cases per year since 1994. During this time period 93% of reported cases for which racial data were available occurred in whites and the median age was six years. In 93% of cases a viral illness had occurred in the preceding three-week period. For the period 1991-1994, the annual rate of hospitalizations due to Reye syndrome in the US was estimated to be between 0.2 and 1.1 per million population less than 18 years of age.

During the 1980s, a case-control study carried out in the United Kingdom also demonstrated an association between Reye syndrome and aspirin exposure. In June 1986, the United Kingdom Committee on Safety of Medicines issued warnings against the use of aspirin in children under 12 years of age and warning labels on aspirin-containing medications were introduced. UK surveillance for Reye syndrome documented a decline in the incidence of the illness after 1986. The reported incidence rate of Reye syndrome decreased from a high of 0.63 per 100,000 population less than 12 years of age in 1983/84 to 0.11 in 1990/91.

From November 1995 to November 1996 in France, a national survey of pediatric departments for children under 15 years of age with unexplained encephalopathy and a threefold (or greater) increase in serum aminotransferase and/or ammonia led to the identification of nine definite cases of Reye syndrome (0.79 cases per million children). Eight of the nine children with Reye syndrome were found to have been exposed to aspirin. In part because of this survey result, the French Medicines Agency reinforced the international attention to the relationship between aspirin and Reye syndrome by issuing its own public and professional warnings about this relationship.