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Functional Neurologic Disorder Wikipedia

Wessely and White have argued that FND may merely be an unexplained somatic illness (like fibromyalgia, irritable bowel syndrome, or chronic fatigue syndrome) single disorder than separate disorders. [28] References [ edit ] ^ a b Carson, A.; et al.
Ritscher-Schinzel Syndrome GeneReviews

Leonardi et al [2001] suggested minimal clinical diagnostic criteria based on 28 affected individuals reported in the literature.

WASHC5, CCDC22, DPH1, TBX1
- Ritscher-Schinzel Syndrome 2 OMIM
  
  A number sign (#) is used with this entry because of evidence that Ritscher-Schinzel syndrome-2 (RTSC2) is caused by mutation in the CCDC22 gene (300859) on chromosome Xp11. Description Ritscher-Schinzel syndrome-2 is an X-linked recessive syndromic form of intellectual disability associated with posterior fossa defects, cardiac malformations, and minor abnormalities of the face and distal extremities (summary by Kolanczyk et al., 2015). For a discussion of genetic heterogeneity of Ritscher-Schinzel syndrome, see RTSC1 (220210). Clinical Features Voineagu et al. (2012) reported a large family (IGOLD #586) in which 6 males spanning 3 generations had syndromic X-linked intellectual disability. One patient was deceased; clinical information was available for 5 patients, but the information given in a table was somewhat variable and unclear as to which individual had which features.
- 3c Syndrome Orphanet
  
  Cranio-cerebello-cardiac (3C) syndrome is a rare multiple congenital anomalies syndrome characterized by craniofacial (prominent occiput and forehead, hypertelorism, ocular coloboma, cleft palate), cerebellar (Dandy-Walker malformation, cerebellar vermis hypoplasia) and cardiac (tetralogy of Fallot, atrial and ventricular septal defects) anomalies (see these terms). Epidemiology To date < 50 cases have been described. The syndrome appears to be panethnic. Clinical description 3C syndrome is a congenital disorder characterized by distinctive craniofacial features including, in decreasing frequency, low-set ears, hypertelorism, down-slanting palpebral fissures, depressed nasal bridge, prominent occiput, prominent forehead, cleft palate, micrognathia, ocular coloboma. Additional craniofacial features encompass nevus flammeus (on forehead), low posterior hairline, sparse scalp hair, eyebrows and eyelashes, open mouth with protruding tongue, and short neck. In 80% of cases, cerebellar anomalies are present and include primarily Dandy-Walker malformation or Dandy-Walker variant, cerebellar vermis hypoplasia and enlargement of cisterna magma.
- 3c Syndrome Wikipedia
  
  3C syndrome Other names CCC dysplasia , Craniocerebellocardiac dysplasia [1] or Ritscher–Schinzel syndrome , [2] Specialty Medical genetics 3C syndrome is a rare condition whose symptoms include heart defects , cerebellar hypoplasia , and cranial dysmorphism . It was first described in the medical literature in 1987 by Ritscher and Schinzel, for whom the disorder is sometimes named. Contents 1 Signs and symptoms 2 Genetics 3 Diagnosis 3.1 Differential diagnosis 4 Management 5 Prognosis 6 Epidemiology 7 History 8 Other animals 9 References 10 External links Signs and symptoms [ edit ] The classical triad of symptoms that defines 3C syndrome includes certain heart defects, hypoplasia (underdevelopment) of the cerebellum , and cranial dysmorphisms, which can take various forms. The heart defects and cranial dysmorphisms are heterogeneous in individuals who are all classed as having Ritscher-Schinzel syndrome. [2] Heart defects commonly seen with Ritscher-Schinzel syndrome are associated with the endocardial cushion and are the most important factor in determining a diagnosis. The mitral valve and tricuspid valve of the heart can be malformed, the atrioventricular canal can be complete instead of developing into the interatrial septum and interventricular septum , and conotruncal heart defects , which include tetralogy of Fallot , double outlet right ventricle , transposition of the great vessels , [2] and hypoplastic left heart syndrome .
- Ritscher-Schinzel Syndrome 1 OMIM
  
  A number sign (#) is used with this entry because Ritscher-Schinzel syndrome-1 (RTSC1) is caused by homozygous mutation in the KIAA0196 gene (WSHC5; 610657) on chromosome 8q24. Description The 3C syndrome, also known as Ritscher-Schinzel syndrome, is a developmental malformation syndrome characterized by craniofacial abnormalities, congenital heart defects, and cerebellar brain malformations. Facial features include prominent occiput, prominent forehead, low-set ears, downslanting palpebral fissures, depressed nasal bridge, and micrognathia. Cardiac defects can include septal defects and aortic stenosis, among others, and brain imaging shows Dandy-Walker malformation, cerebellar vermis hypoplasia, posterior fossa cysts, and ventricular dilatation. Affected individuals have severe developmental delay (summary by Leonardi et al., 2001; Seidahmed et al., 2011).
Abrasion (Dental) Wikipedia

Chemical [ edit ] The current selection of dentifrice should also be critically analysed and changed to include a less abrasive and gentler paste such as sensitive toothpaste as evidence suggests that a very abrasive toothpaste would lead to loss of tooth structure. [27] A toothpaste containing increased fluoride will also help combat the increased sensitivity and risk to dental decay. [28] Fluoride varnish is known to alleviate hypersensitivity in teeth and can be used as a preventive measure for high risk patients of dental erosion with abrasion because fluoride varnish is reported to have an effect on the surface and subsurface of the tooth. [29] Treatment in the dental chair may include a fluoride application or the placement of a restoration in more severe cases.
Micropsia Wikipedia

This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. [26] Laser treatments also look promising but are still in clinical stages. [26] Epidemiology [ edit ] Episodes of micropsia or macropsia occur in 9% of adolescents. [27] 10-35% of migraine sufferers experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras. [28] Micropsia seems to be slightly more common in boys than in girls among children who experience migraines. [29] Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia.

ATXN7, TTPA, CLN6, TSEN34, TSEN2, TSEN54
Bovine Viral Diarrhea Wikipedia

Vaccination [ edit ] Modern vaccination programmes aim not only to provide a high level of protection from clinical disease for the dam, but, crucially, to protect against viraemia and prevent the production of PIs. [28] While the immune mechanisms involved are the same, the level of immune protection required for foetal protection is much higher than for prevention of clinical disease. [29] While challenge studies indicate that killed, as well as live, vaccines prevent foetal infection under experimental conditions, the efficacy of vaccines under field conditions has been questioned. [30] The birth of PI calves into vaccinated herds suggests that killed vaccines do not stand up to the challenge presented by the viral load excreted by a PI in the field. [31] See also [ edit ] Animal viruses References [ edit ] ^ a b c d Fray; et al. (2000).
Central Nervous System Disease Wikipedia

., Lorazepam ) in pill and I.V. form. [28] Depression [ edit ] Main article: Major depressive disorder Major depressive disorder, otherwise known as depression, is a disorder that is characterized by a pervasive and persistent low mood that is accompanied by low self-esteem and by a loss of interest or pleasure in normally enjoyable activities.

EPO, IDH2, IL17A, SOD2, BDNF, MOG, GFAP, GSK3B, AQP4, GRM5, HMOX1, IL6, TSPO, NFE2L2, NLRP3, APOE, P2RX7, PDE4A, APP, ALK, PARP1, MMP9, GABPA, ABCB1, PDE10A, PLP1, PDXP, CYP2D6, IL33, SLC6A3, PTHLH, CSF2, CCL2, PRDX5, TNF, ERBB2, LAMC2, PRNP, CXCR3, USP18, GCG, HRH3, FGF2, LPAR3, GPR42, SSTR4, GRN, GRM1, MAPK3, KEAP1, LPAR2, ICAM1, IFNG, FZD4, EGFR, CXCL8, KCNK2, TTC4, TRPM2, TRAF6, TLR4, HTR1A, CXCR6, MRGPRX1, ADRA1A, MRGPRX4, CD44, EDNRA, CCR5, GPR151, BRS3, BRAF, OXER1, GPRC6A, LGR6, CSF1R, CSF3, ADRA2B, ACKR3, MRGPRX3, GPR166P, VN1R17P, WWOX, ATN1, RSS, REN, TNFRSF1A, TNFRSF1B, RAG1, NPS, TSHR, CD200R1, RAC2, SGSH, ADGRG3, TXN, NR1H2, VCP, RBM45, VEGFA, BHLHE23, VIM, PTPRZ1, PTPN6, TTR, TLR2, MIR34A, TIMP1, SLC6A4, SLC6A9, CXCL12, SMS, SNCA, SOD1, MIR21, MIR132, GTF2H5, SPP1, SST, SCN2A, MTDH, ROS1, SYN1, TACR1, TCF4, TGFB1, TGIF1, PSAT1, KRT90P, XPA, ZFP36, PTEN, NGB, EBP, CYSLTR1, SLC12A5, RIPK3, TPPP, PTPRT, NDRG2, PDCD10, GJC2, ELP2, FEZF2, MGLL, MPRIP, SLC52A1, CYFIP1, BRD4, PANX1, TREM2, SAMHD1, ADGRA2, ELP4, GPR88, TMEM97, CXCL13, SIGMAR1, BCAP31, XPR1, CXCR4, NR0B2, ITGA10, RIPK1, NR1I2, ORAI1, MEGF10, SOCS3, CH25H, PLVAP, MYOM2, CD276, NYX, PNMA1, ADIPOQ, ABCG2, ROCK2, ADAMTS4, ADAMTS3, NPEPPS, RTN4R, VSIR, SV2A, HDAC6, AAVS1, OAS3, PTAFR, ESR2, CYP2B6, CYP2C9, CYP3A4, ACE, DDIT3, DRD2, TSC22D3, TOR1A, ECHS1, EDNRB, ELF2, ERCC2, ERCC3, ERN1, EWSR1, GRIN2B, F2R, F2RL1, FANCB, FPR2, MTOR, GAD2, GC, GDF2, GIP, GJA1, GLB1, GLP1R, GNA12, GPR3, CYP1A2, CTSS, CST3, CSF1, ACHE, ACTB, ADAM8, ADORA2A, AGT, AGTR1, AGTR2, KLK3, ARSB, ALDH7A1, BCL2, DST, SERPING1, C5, C5AR1, CACNA1D, CAV1, CD19, CD34, CD36, CD38, CDH11, CHAT, CHRNA4, CNR2, CNTF, ATF2, CRH, CRHBP, GPR17, GRM3, KLK6, PDE1C, MME, MMP2, MMP12, CD200, MST1R, MYCL, MYD88, NCAM1, NEFL, NPC1, NTS, OAS2, ASIC1, OPRK1, PDE4B, GRM4, PDE4D, PGR, SERPINA1, SERPINI1, PIK3CD, PLAG1, PMP22, POMC, PPARA, PPARG, MAPK8, MAP2K7, PROS1, LGMN, NR3C2, MGAT1, MEF2C, CD46, GRM7, GRP, GTF2H1, GTF2H2, GTF2H3, GTF2H4, HINT1, HLA-DRB1, HMGB1, HMGCR, NR4A1, HP, HSPA9, HTR2A, HTR2C, IDS, IDUA, IFNA1, IFNA13, IGF1, IGHM, IL1B, IL3, CXCL10, L1CAM, MAOB, MAPT, MBL2, MBP, CCR2
Neuroinflammation Wikipedia

Current treatments for multiple sclerosis include interferon-B, Glatiramer acetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression [28] In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease.
Cyclic Vomiting Syndrome Wikipedia

"Cyclic vomiting syndrome: epidemiology, diagnosis, and treatment". Clinical Autonomic Research . 28 (2): 203–209. doi : 10.1007/s10286-018-0506-2 .

TRNL1, MMP9, IL6, ADM, PCYT1A, MIR15A, RETN, KLF4, TIMP3, ACSM3, S100B, S100A1, RYR2, PTGS2, PPARG, NOS2, OPRM1, AFP, NOS1, MMP3, IL1B, IL1A, ICAM1, HMGB1, GJA1, EDN1, CNR1, CERNA3
- Cyclic Vomiting Syndrome Mayo Clinic
  
  Overview Cyclic vomiting syndrome is characterized by episodes of severe vomiting that have no apparent cause. Episodes can last for hours or days and alternate with symptom-free periods. Episodes are similar, meaning that they tend to start at the same time of day, last the same length of time, and occur with the same symptoms and intensity. Cyclic vomiting syndrome occurs in all age groups, though it often begins in children around 3 to 7 years old. Although it's more common in children, the number of cases diagnosed in adults is increasing.
- Cyclic Vomiting Syndrome MedlinePlus
  
  Cyclic vomiting syndrome is a disorder that causes recurrent episodes of nausea, vomiting, and tiredness (lethargy). This condition is diagnosed most often in young children, but it can affect people of any age. The episodes of nausea, vomiting, and lethargy last anywhere from an hour to 10 days. An affected person may vomit several times per hour, potentially leading to a dangerous loss of fluids (dehydration). Additional symptoms can include unusually pale skin (pallor), abdominal pain, diarrhea, headache, fever, and an increased sensitivity to light (photophobia) or to sound (phonophobia).
- Cyclic Vomiting Syndrome OMIM
  
  A number sign (#) is used with this entry because of evidence that cyclic vomiting syndrome can be caused by mutation in the mitochondrial transfer RNA-leucine gene (MTTL1; 590050). Clinical Features Cyclic vomiting syndrome has long been recognized (Lombard, 1861; Gee, 1882). It is characterized by recurrent, explosive bouts of vomiting punctuated by periods of normal health. Affected individuals have stereotypical episodes with rapid onset, most often during the night or in the early morning, a high peak frequency of vomiting every 10 to 15 minutes, associated with nausea, retching, abdominal pain, lethargy, anorexia, pallor, and a rapid complete resolution. Median age at onset is 5 years, and median age at resolution of symptoms is 10 years (Haan et al., 2002).
Duarte Galactosemia Wikipedia

The first [12] report published in 2008 was a pilot study that looked at biochemical markers and developmental outcomes in a group of 28 toddlers and young children with DG, some of whom had drunk milk through infancy and some of whom had drunk low-galactose formula.
- Galactosemia MedlinePlus
  
  Galactosemia is a disorder that affects how the body processes a simple sugar called galactose. A small amount of galactose is present in many foods. It is primarily part of a larger sugar called lactose, which is found in all dairy products and many baby formulas. The signs and symptoms of galactosemia result from an inability to use galactose to produce energy. Researchers have identified several types of galactosemia. These conditions are each caused by mutations in a particular gene and affect different enzymes involved in breaking down galactose. Classic galactosemia, also known as type I, is the most common and most severe form of the condition.
Viral Meningitis Wikipedia

For herpes the treatment of choice is aciclovir . [28] If encephalitis is suspected, empiric treatment with IV aciclovir is often warranted. [16] Surgical management is indicated where there is extremely increased intracranial pressure, infection of an adjacent bony structure (e.g. mastoiditis ), skull fracture, or abscess formation. [12] The majority of people that have viral meningitis get better within 7–10 days. [29] Epidemiology [ edit ] From 1988–1999, about 36,000 cases occurred each year. [30] As recently as 2017, the incidence in the U.S. alone increased to 75,000 cases per year for enteroviral meningitis. [10] With the advent and implementation of vaccinations for organisms such as Streptococcus pneumoniae, Haemophilus influenza type B, and Neisseria meningitis , rates of bacterial meningitis have been in decline, making viral meningitis more common. [16] Countries without high rates of immunization still carry higher rates of bacterial disease. [16] While the disease can occur in both children and adults, it is more common in children. [1] Rates of infection tend to reach a peak in the summer and fall. [31] During an outbreak in Romania and in Spain viral meningitis was more common among adults. [32] While, people aged younger than 15 made up 33.8% of cases. [32] In contrast in Finland in 1966 and in Cyprus in 1996, Gaza 1997, China 1998 and Taiwan 1998, the incidences of viral meningitis were more common among children. [33] [34] [35] [36] Recent research [ edit ] It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall . [37] The Meningitis Research Foundation is conducting a study to see if new genomic techniques can improve the speed, accuracy and cost of diagnosing meningitis in children in the UK.

CSF2, LAMC2, IL6, CXCL8, MMP9, TIMP1, CD19, CRP, ENO2, ICAM1, MMP2, TGFB1, TIMP2, CXCL13
Auditory Fatigue Wikipedia

As blood temperature rises, TTS increases when paired with high-frequency noise exposure. [12] It is hypothesized that hair cells for high-frequency transduction require a greater oxygen supply than others, and the two simultaneous metabolic processes can deplete any oxygen reserves of the cochlea. [27] In this case, the auditory system undergoes temporary changes caused by a decrease in the oxygen tension of the cochlear endolymph that leads to vasoconstriction of the local vessels. [28] Further research could be done to see if this is a reason for the increased TTS during physical exercise that is during continued noise-exposure as well.
Purpura Fulminans Wikipedia

History [ edit ] Purpura fulminans was first described by Guelliot in 1884. [28] References [ edit ] ^ James, William D.; Berger, Timothy G.; et al. (2006).

PROC, PC, SLC25A10, F5, PROS1, F2, ADAM10, APC, DNAH5, PCBD1, PRH1, PRH2, PROCR, DNAI1, DNAAF3
Iminoglycinuria Wikipedia

Here, cotransporters such as sodium or chloride (part of the system of Na-K-Cl cotransporters ) couple with the amino or imino acids on the molecular level and transport them through specific integral membrane proteins that form ion channels , which are located within the cell membrane . [27] [28] From the cells, the absorbed or reabsorbed amino and imino acids eventually reach the blood.

SLC6A19, SLC36A2, SLC6A20, SLC6A18
- Iminoglycinuria Orphanet
  
  A rare inborn error of metabolism characterized by elevated levels of imino acids (proline, hydroxyproline) and glycine in urine due to defective reabsorption in the kidney. The condition is considered benign and not associated with any specific clinical phenotype. Mode of inheritance is autosomal recessive.
- Iminoglycinuria OMIM
  
  A number sign (#) is used with this entry because of evidence that iminoglycinuria is a digenic phenotype that can be caused by homozygous mutation in the SLC36A2 gene (608331) combined with heterozygous mutation in the SLC6A20 gene (605616) or homozygous mutation in the SLC6A19 gene (608893). Description The imino acids, proline and hydroxyproline, share a renal tubular reabsorptive mechanism with glycine. Iminoglycinuria (IG), a benign inborn error of amino acid transport, is also a normal finding in neonates and infants under 6 months of age (Chesney, 2001). Early studies of families with iminoglycinuria suggested genetic complexity, with homozygotes developing IG and heterozygotes manifesting only hyperglycinuria (HG; 138500) (summary by Broer et al., 2008). Iminoglycinuria may be more frequent in Ashkenazim than in others (Tancredi et al., 1970).
Abortion In South Korea Wikipedia

. ^ a b c d e f "South Korea: Stop criminalization of abortion" . Amnesty International . 28 October 2016. doi : 10.1163/2210-7975_hrd-9211-2016094 .
Limited-Stage Small Cell Lung Carcinoma Wikipedia

Comparing to continued smokers, patients who quit at or after diagnosis lower the risk of death by 45%. [28] References [ edit ] ^ a b c Stinchcombe TE, Gore EM (2010).
Hemiballismus Wikipedia

"Hemichorea-hemiballismus may respond to topiramate". Clinical Neuropharmacology . 28 (3): 142–144. doi : 10.1097/01.wnf.0000164160.71206.a3 .

CP, DRD2, HTR2A, OPRM1, PDYN, PPP1R1B, PDE10A, LRP2, MCF2L
Atopy Wikipedia

In addition, several studies have documented that an IgE-mediated response to S. aureus is present in people with atopic eczema. [27] [28] Changes in prevalence [ edit ] In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. [29] However, the biological reasons for these changes are not fully understood.

MAP3K5, SLC19A1, CEP350, FNDC3A, BBS9, COL6A5
Soil-Transmitted Helminthiasis Wikipedia

. ^ "Neglected Tropical Diseases" . cdc.gov . June 6, 2011 . Retrieved 28 November 2014 . ^ London Declaration (2012) (30 January 2012).
Genital Wart Wikipedia

. ^ a b c d e f g h i "CDC - Genital Warts - 2010 STD Treatment Guidelines" . www.cdc.gov . 28 January 2011. Archived from the original on 8 July 2018 .

TP53, PDXP, CDKN2A, IFNB1, IL10, PIK3CG, PIK3CA, PIK3CB, IFNG, IFNA13, IFNA1, PIK3CD, ZAP70, BCL2, SULT2A1, JUN, NDRG1, PYCARD, ARTN, NR0B2, UBL4A, WNT1, VEGFA, YAP1, PDZD2, CADM1, AGRP, CD274, IL22, FOXP3, DNAJA4, PNPLA2, MIB1, IL21, BIRC7, IL33, MPEG1, MIR99B, HNP1, MIR551B, DEFA1B, DEFB4B, TTK, PTPN11, TGFB1, IL6, XIAP, STS, DEFA1, DEFB4A, EGFR, FCGRT, G6PD, GLB1, ICAM3, IDUA, IGF1R, IL2, IL18, STAT2, CXCL10, JAK1, MBL2, MKI67, PCNA, SERPINF1, PIN1, PTPN6, BIRC3, RPS27, XCL1, STAT1, H3P10
- Genital Warts Mayo Clinic
  
  Overview Genital warts are one of the most common types of sexually transmitted infections. Nearly all sexually active people will become infected with at least one type of human papillomavirus (HPV), the virus that causes genital warts, at some point during their lives. Genital warts affect the moist tissues of the genital area. They can look like small, flesh-colored bumps or have a cauliflower-like appearance. In many cases, the warts are too small to be visible. Some strains of genital HPV can cause genital warts, while others can cause cancer. Vaccines can help protect against certain strains of genital HPV . Symptoms In women, genital warts can grow on the vulva, the walls of the vagina, the area between the external genitals and the anus, the anal canal, and the cervix.
Congenital Heart Block Wikipedia

See also: Neonatal lupus erythematosus Congenital heart block The conduction system of the heart (shown in yellow) Specialty Medical genetics Symptoms slow heart rate [1] Usual onset in utero. [1] Diagnostic method fetal echocardiogram and Doppler and ELISA for the mother [1] Treatment fluorinated steroids, beta agonists, IVIG, HCQ, pace maker implantation and maternal plasmapheresis. [1] [2] Frequency 1 child in every 15000-20000 [3] The congenital heart block ( CHB ) is the heart block that is diagnosed in fetus ( in utero ) or within the first 28 days after birth [1] [4] (neonatal period), some studies also include the diagnosis during early childhood to the definition of CHB. [5] It refers to the disorder in the electrical conduction system within the heart muscle, [4] which leads to the failure in pumping the blood efficiently into the aorta and the pulmonary trunk .
- Heart Block, Congenital OMIM
  
  A rather large number of families with multiple affected sibs and normal parents have been reported. Latta and Crittenden (1964) studied the hearts of 2 sibs (the seventh and eighth offspring) who died neonatally of congenital heart block. In neither was an atrioventricular node found, nor were myocardial fibers present in the lower part of the interatrial septum. Both hearts showed foci of calcification, fibrosis, increased vascularization and a few small accumulations of inflammatory cells. Thus, fetal infection (or autoimmune reaction, as discussed later) could have been responsible.