It did not pass. [26] In 2019, women in Colorado were eligible for temporary disability as a result of abortion or miscarriage. [27] [28] Judicial history [ edit ] The US Supreme Court 's decision in 1973's Roe v. ... The Denver Post . 2017-12-01 . Retrieved 2019-05-28 . ^ a b c d "Abortion Incidence and Services in the United States, 1995-1996" . ... Retrieved 2019-05-25 . ^ Low, Matt Donnelly,Gene Maddaus,Elaine; Donnelly, Matt; Maddaus, Gene; Low, Elaine (2019-05-28). "Netflix the Only Hollywood Studio to Speak Out in Attack Against Abortion Rights (EXCLUSIVE)" .
If the uterus has been irreparably damaged, surrogacy or adoption may be the only options. [ citation needed ] Depending on the degree of severity, AS may result in infertility , repeated miscarriages , pain from trapped blood, and future obstetric complications [13] If left untreated, the obstruction of menstrual flow resulting from adhesions can lead to endometriosis in some cases. [3] [27] Patients who carry a pregnancy even after treatment of IUA may have an increased risk of having abnormal placentation including placenta accreta [28] where the placenta invades the uterus more deeply, leading to complications in placental separation after delivery. ... For women under 35 years of age treated for severe adhesions, pregnancy rates were 66.6% compared to 23.5% in women older than 35. [28] Epidemiology [ edit ] AS has a reported incidence of 25% of D&Cs performed 1–4 weeks post-partum, [27] [9] [32] up to 30.9% of D&Cs performed for missed miscarriages and 6.4% of D&Cs performed for incomplete miscarriages. [33] In another study, 40% of patients who underwent repeated D&C for retained products of conception after missed miscarriage or retained placenta developed AS. [34] In the case of missed miscarriages, the time period between fetal demise and curettage may increase the likelihood of adhesion formation due to fibroblastic activity of the remaining tissue. [8] [35] The risk of AS also increases with the number of procedures: one study estimated the risk to be 16% after one D&C and 32% after 3 or more D&Cs. [17] However, a single curettage often underlies the condition. In an attempts to estimate the prevalence of AS in the general population, it was found in 1.5% of women undergoing hysterosalpingography HSG, [36] and between 5 and 39% of women with recurrent miscarriage. [37] [38] [39] After miscarriage, a review estimated the prevalence of AS to be approximately 20% (95% confidence interval : 13% to 28%). [14] History [ edit ] The condition was first described in 1894 by Heinrich Fritsch (Fritsch, 1894) [40] [41] and further characterized by the Czech - Israeli gynecologist Joseph Asherman (1889–1968) [42] in 1948. [43] It is also known as Fritsch syndrome, or Fritsch-Asherman syndrome.
In the case of anti-c, the woman should be checked around 28 weeks to see if she has developed anti-E as well. [ citation needed ] Mother [ edit ] Blood testing for the mother is called an Indirect Coombs Test (ICT) or an Indirect Agglutination Test (IAT). ... IVIG and plasmapheresis together can reduce or eliminate the need for an IUT. [26] Plasmapheresis - Plasmapheresis aims to decrease the maternal titer by direct plasma replacement. [27] Plasmapheresis and IVIG together can even be used on women with previously hydropic fetuses and losses. [28] [29] Mid to late pregnancy [ edit ] IUT - Intrauterine transfusion (IUT) is done either by intraperitoneal transfusion (IPT) or intravenous transfusion (IVT). [30] IVT is preferred over IPT. [15] IUTs are only done until 35 weeks. ... Ultrasound in Obstetrics and Gynecology . 28 (6): 814–20. doi : 10.1002/uog.2837 .
Indonesia [ edit ] Main article: HIV/AIDS in Indonesia UNAIDS has said that HIV/AIDS in Indonesia is one of Asia's fastest growing epidemics. [28] It was expected that 5 million Indonesians would have HIV/AIDS by 2010. [29] In 2007, Indonesia was ranked 99th in the world by prevalence rate , but because of low understanding of the symptoms of the disease and high social stigma attached to it, only 5–10% of HIV/AIDS sufferers were diagnosed and treated. [29] Laos [ edit ] Main article: HIV/AIDS in Laos In 2005, UNAIDS estimated that 3,700 people in Lao PDR were living with HIV. [30] Lao PDR currently faces a concentrated epidemic with an adult HIV prevalence of 0.1%. ... CS1 maint: archived copy as title ( link ) ^ "Data of 14,200 people with HIV leaked online by American fraudster:MOH" . The Business Times . January 28, 2019. ^ hermesauto (2019-01-28).
For example, in some OPA1 carriers, patients will develop neurological features indistinguishable from HSP while others develop a pattern of peripheral neuropathy with a similar disease course to CMT, and still others will develop a prominent cerebellar syndrome consistent with FRDA. [21] Pathophysiology [ edit ] Even though dysfunction of the mitochondria can be either congenital or acquired, both causes share a common pathophysiology : an impairment of oxidative phosphorylation within the mitochondria, which leads to a decrease of ATP production and a simultaneous increase in ROS . [28] These mitochondria are made within the central somata of the retinal ganglion cell, transported down axons , and distributed where they are needed. ... Journal of the Neurological Sciences . 127 (1): 11–28. doi : 10.1016/0022-510x(94)90130-9 . ... Biochimica et Biophysica Acta (BBA) - Bioenergetics . 1787 (5): 518–28. doi : 10.1016/j.bbabio.2009.02.024 .
Whilst this is typically carried out by craniotomy , a new endoscopic endonasal approach is being trialled. [28] Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. [29] After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping. [30] Endovascular coiling [ edit ] Main article: Endovascular coiling Endovascular coiling refers to the insertion of platinum coils into the aneurysm. ... "Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage". Neurological Research . 28 (7): 750–58. doi : 10.1179/016164106X152025 . ... "Case-Fatality Rates and Functional Outcome After Subarachnoid Hemorrhage : A Systematic Review". Stroke . 28 (3): 660–64. doi : 10.1161/01.STR.28.3.660 .
Please improve this section by adding secondary or tertiary sources . ( December 2020 ) ( Learn how and when to remove this template message ) Shortly after PLOS One published the corrected study, a critique of the original study's methodology appeared in Archives of Sexual Behavior . [28] In a letter to the editor, Littman responded with a side-by-side comparison, stating that the criticized methodologies were consistent with those that had been used, without controversy, in widely-cited studies supporting gender identity affirmation health care. [29] A number of clinicians who provide care for gender dysphoric youth state that what was described in Littman's research is consistent with their patient population. [30] [31] [ better source needed ] [32] Several additional reports published since the PLOS article republication note a novel large adolescent cohort presenting with gender dysphoria. [33] [34] [35] [36] There is speculation about the reasons for the observed increased incidence, including more available treatment, increased awareness or influence via social media and the internet, and increased societal acceptance of gender identity variance. [35] Professional commentary [ edit ] Following publication of the original report in PLOS One , the World Professional Association for Transgender Health (WPATH) released a position paper on the proposed term "rapid onset gender dysphoria" and the research, stating that the term is not recognized by any professional association, nor listed in the DSM or ICD lists of disorders and diseases. ... PMID 30889187 . ^ Rudgard, Olivia (August 28, 2018). "Brown University in row with transgender activists over claims gender dysphoria spreading among children" . ... Archived from the original on 2018-08-28. ^ Paxson, Christina (September 9, 2018).
Conceptualization [ edit ] In a series of publications, [27] [28] [29] philosopher Paul Franceschi has proposed a unified conceptual framework for cognitive distortions designed to clarify their relationships and define new ones. ... PsychCentral . 2016-05-17 . Retrieved 2020-02-28 . ^ "Fallacy of Change: 15 types of distorted thinking that lead to massive anxiety 10/15" . ... "Preoperative Anxiety and Catastrophizing". The Clinical Journal of Pain . 28 (9): 819–841. doi : 10.1097/ajp.0b013e31824549d6 .
The addition of rituximab to chemotherapy regimens such as CHOP has greatly improved the prognosis of most DLBCL variants [22] and modestly improved the outcome in patients with the Epstein–Barr virus-positive diffuse large B-cell lymphoma, not otherwise specified variant of DLBCL. [27] [28] There are too few reports on the treatment of non-PAL forms of DLBCL-CI to make recommendations although the R-CHOP regimen is being used as first-line treatment for severe DLBCL-CI cases that are not PAT. [29] [25] The R-CHOP regiment or similar immunochemotherapeutic regimen (e.g. ... "How compelling are the data for Epstein-Barr virus being a trigger for systemic lupus and other autoimmune diseases?". Current Opinion in Rheumatology . 28 (4): 398–404. doi : 10.1097/BOR.0000000000000289 . ... Pathogens (Basel, Switzerland) . 7 (1): 28. doi : 10.3390/pathogens7010028 .
There are 54 known keratin genes—of which 28 belong to the type I intermediate filament genes and 26 to type II—which work as heterodimers . ... Carrier frequency ranges from 1 in 333 for JEB, to 1 in 450 for DEB; the carrier frequency for EBS is presumed to be much higher than JEB or DEB. [ citation needed ] The disorder occurs in every racial and ethnic group and affects both sexes. [25] [26] Society and culture [ edit ] In 2010, Emma Fogarty, a campaigner for DEBRA Ireland (the EB charity) was awarded a People of the Year Award . [27] Actor Colin Farrell has campaigned with Fogarty on behalf of sufferers. [28] In 2014, Pearl Jam lead vocalist Eddie Vedder together with his wife Jill McCormick co-founded the EB Research Partnership, [29] a non-profit organization dedicated to finding a cure for epidermolysis bullosa. [30] McCormick is childhood friends with Ryan Fullmer, whose son, Michael, was born with EB. ... Channel 4 . 2004 . Retrieved 2009-02-28 . ^ Butterfly Girl: Remembering Abigail Evans , The Austinot, January 12, 2015. ^ Andrew Duffy, "TSN documentary on Jonathan Pitre wins screen award" .
Overview Epidermolysis bullosa (ep-ih-dur-MOL-uh-sis buhl-LOE-sah) is a rare condition that causes fragile, blistering skin. The blisters may appear in response to minor injury, even from heat, rubbing or scratching. In severe cases, the blisters may occur inside the body, such as the lining of the mouth or stomach. Epidermolysis bullosa is inherited, and it usually shows up in infants or young children. Some people don't develop symptoms until they're teens or young adults.
Epidermolysis bullosa (EB) is a group of genetic skin diseases that cause the skin to blister and erode very easily. In people with EB, blisters form in response to minor injuries or friction, such as rubbing or scratching.[2310] There are four main types of EB, which are classified based on the depth, or level, of blister formation: Epidermolysis bullosa simplex Dystrophic epidermolysis bullosa Junctional epidermolysis bullosa Kindler Syndrome EB may then be further classified based on severity and specific symptoms, such as distribution (localized or generalized) and whether parts of the body other than the skin are affected. Specific sub-types may then be determined based on identifying the exact protein that is defective in a person with EB. This may be done by tests performed on a skin biopsy, or when possible, genetic testing. Identifying the exact sub-type can be hard because there are many sub-types of EB.
The rate of comorbidity of OCPD in patients with OCD is estimated to be around 15-28%. [20] However, due to the addition of the hoarding disorder diagnosis in the DSM-5, and studies showing that hoarding may not be a symptom of OCPD, the true rate of comorbidity may be much lower. [20] There is significant similarity in the symptoms of OCD and OCPD, which can lead to complexity in distinguishing them clinically. ... A researcher in 1949 described the behavior of the average “anorexic girl” as being "rigid" and "hyperconscious", observing a tendency to "[n]eatness, meticulosity, and a mulish stubbornness not amenable to reason [which] make her a rank perfectionist". [28] Other disorders and conditions [ edit ] A diagnosis of OCPD is common with anxiety disorders , substance use disorders , and mood disorders . [4] OCPD is also highly comorbid with Cluster A personality disorders , [4] Psychiatric disorder Prevalence of OCPD in 12 month diagnosis [4] Substance use disorder 12–25% Mood disorders 24% Major depressive disorder 23–28% Bipolar disorder 26–39% Anxiety disorders 23–24% Generalised anxiety disorder 34% Panic disorder 23–38% Social anxiety disorder 33% Specific phobia 22% especially paranoid and schizotypal personality disorders. [4] OCPD has also been linked to a higher relapse in those who are treated for major depressive disorder , [29] and a higher risk of suicidal behaviour. [29] The table on the left shows the comorbidity rates for OCPD among each psychiatric disorder listed.
Lymphocytic infiltration of the thyrocyte -associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland. [ citation needed ] Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it. [28] Treatment [ edit ] Managing hormone levels [ edit ] Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine , triiodothyronine , or desiccated thyroid extract . ... Department of Health and Human Services. 12 June 2017. Archived from the original on 28 July 2017 . Retrieved 17 July 2017 . ... "The CD40, CTLA-4, thyroglobulin, TSH receptor, and PTPN22 gene quintet and its contribution to thyroid autoimmunity: Back to the future" . Journal of Autoimmunity . 28 (2–3): 85–98. doi : 10.1016/j.jaut.2007.02.006 .
Hashimoto thyroiditis is a condition that affects the function of the thyroid, which is a butterfly-shaped gland in the lower neck. The thyroid makes hormones that help regulate a wide variety of critical body functions. For example, thyroid hormones influence growth and development, body temperature, heart rate, menstrual cycles, and weight. Hashimoto thyroiditis is a form of chronic inflammation that can damage the thyroid, reducing its ability to produce hormones. One of the first signs of Hashimoto thyroiditis is an enlargement of the thyroid called a goiter.
In a family with several cases of Hashimoto struma, DeGroot et al. (1962) demonstrated an abnormal, small, iodinated protein in the serum and suggested that a defect in thyroid basement membrane may account for the appearance of this protein in the blood. Three sibs, their father, and their paternal aunt were affected. The paternal grandparents were dead. Hall et al. (1962) presented data that they felt supported autosomal dominant inheritance of the tendency to thyroid autoimmunity. Hall et al. (1964) studied 6 families in which the father had thyroid autoantibody and the mother did not. In each case female children had thyroid autoantibodies. Transplacental transmission was thus ruled out and genetic transmission was suggested.
Overview Hashimoto's disease is an autoimmune disorder affecting the thyroid gland. The thyroid is a butterfly-shaped gland located at the base of the neck just below the Adam's apple. The thyroid produces hormones that help regulate many functions in the body. An autoimmune disorder is an illness caused by the immune system attacking healthy tissues. In Hashimoto's disease, immune-system cells lead to the death of the thyroid's hormone-producing cells.
Some of the recessive forms have been associated with defects in proteins that make up the dystrophin-glycoprotein complex. [12] Though a person normally leads a normal life with some assistance, in some extreme cases, death from LGMD occurs due to cardiopulmonary complications. [27] Myotonic muscular dystrophy 160900 , 602668 DMPK , ZNF9 Myotonic muscular dystrophy is an autosomal dominant condition that presents with myotonia (delayed relaxation of muscles), as well as muscle wasting and weakness. [28] Myotonic MD varies in severity and manifestations and affects many body systems in addition to skeletal muscles, including the heart, endocrine organs, and eyes. [29] Myotonic MD type 1 (DM1) is the most common adult form of muscular dystrophy. ... Spontaneous mutations . [ page needed ] ^ "DMD gene" . Genetics Home Reference . 2016-03-28. Archived from the original on 2016-04-16 . ... Retrieved 2017-03-14 . ^ Rosenberg, Roger N.; Pascual, Juan M. (2014-10-28). Rosenberg's Molecular and Genetic Basis of Neurological and Psychiatric Disease . p. 1174.
Congenital muscular dystrophy (CMD) is a heterogeneous group of neuromuscular disorders with onset at birth or infancy characterized by hypotonia, muscle wasting, weakness or delayed motor milestones. The group includes myopathies with abnormalities at different cellular levels: the extracellular matrix (MDC1A, UCMD; see these terms), the dystrophin-associated glycoprotein complex (alphadystroglycanopathies, integrinopathies see these terms), the endoplasmic reticulum (rigid spine syndrome [RSMD1], and the nuclear envelope (LMNA-related CMD; [L-CMD] and Nesprin-1-related CMD; see these terms). Epidemiology The prevalence of CMDs is not well known but is estimated at about 1-9/100,000 in countries where they are most frequent. Males and females are equally affected. Clinical description Orthopaedic and respiratory complications that may be life-threatening often develop in the course of the disease. Etiology CMDs have autosomal recessive inheritance with the exception of dominant mutations possible in at least two forms (UCMD may have autosomal dominant or recessive inheritance; L-CMD is due to dominant de novo mutations).
Overview Muscular dystrophy is a group of diseases that cause progressive weakness and loss of muscle mass. In muscular dystrophy, abnormal genes (mutations) interfere with the production of proteins needed to form healthy muscle. There are many kinds of muscular dystrophy. Symptoms of the most common variety begin in childhood, mostly in boys. Other types don't surface until adulthood. There's no cure for muscular dystrophy. But medications and therapy can help manage symptoms and slow the course of the disease.
Muscular dystrophy (MD) refers to a group of more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms of MD are seen in newborns, infants or children, while others have late-onset and may not appear until middle age or later. The disorders differ in terms of the distribution and extent of muscle weakness (some forms of MD also affect cardiac muscle), age of onset, rate of progression, and pattern of inheritance. The prognosis for people with MD varies according to the type and progression of the disorder. There is no specific treatment to stop or reverse any form of MD. Treatment is supportive and may include physical therapy, respiratory therapy, speech therapy, orthopedic appliances used for support, corrective orthopedic surgery, and medications including corticosteroids, anticonvulsants (seizure medications), immunosuppressants, and antibiotics.
Therefore, the disorder is more appropriately referred to as “tendinosis” or “tendinopathy” rather than “tendinitis.” [28] Colour Doppler ultrasound reveals structural tendon changes, with vascularity and hypo-echoic areas that correspond to the areas of pain in the extensor origin. [29] Load-induced non-rupture tendinopathy in humans is associated with an increase in the ratio of collagen III:I proteins, a shift from large to small diameter collagen fibrils, buckling of the collagen fascicles in the tendon extracellular matrix, and buckling of the tenocyte cells and their nuclei. [30] Diagnosis [ edit ] Diagram illustrating tendonitis and tendon rupture Symptoms can vary from aches or pains and local joint stiffness , to a burning that surrounds the whole joint around the inflamed tendon. ... An in vitro model of human tendon healing". Am J Sports Med . 28 (4): 499–505. doi : 10.1177/03635465000280040901 . ... "Low level laser treatment of tendinopathy: a systematic review with meta-analysis" . Photomedicine and Laser Surgery . 28 (1): 3–16. doi : 10.1089/pho.2008.2470 .
Overview Tendinitis is inflammation of the thick fibrous cords that attach muscle to bone. These cords are called tendons. The condition causes pain and tenderness just outside a joint. Tendinitis can occur in any tendon. But it's most common around shoulders, elbows, wrists, knees and heels. Most tendinitis can be treated with rest, physical therapy and medicine to reduce pain. Long-lasting tendon inflammation can cause a tendon to tear. A torn tendon might need surgery.
Known causes for head tilt in domestic animals include: Encephalitozoon cuniculi (or E. cuniculi ) infection in rabbits [28] Inner ear infection Hypothyroidism in dogs [29] Disease of the VIIIth cranial nerve the N. ... "Torticollis". Journal of Child Neurology . 28 (3): 365–378. doi : 10.1177/0883073812469294 . ... "Efficacy of micro current therapy in infants with congenital muscular torticollis involving the entire sternocleidomastoid muscle". Clinical Rehabilitation . 28 (10): 983–91. doi : 10.1177/0269215513511341 .
Description Torticollis is a twisted neck as a result of shortening of sternocleidomastoid muscle. This short and fibrotic muscle pulls the head laterally and rotates the chin and face to the opposite end. Facial asymmetry may be a manifestation (summary by Engin et al., 1997). Clinical Features Thompson et al. (1986) reported 5 girls with congenital muscular torticollis from 3 sibships of an inbred kindred. Engin et al. (1997) described a Turkish family in which 5 patients over 3 generations had congenital muscular torticollis.
By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore. [28] In 2001, Nipah virus was reported from Meherpur District , Bangladesh [29] [30] and Siliguri , India. [29] The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District , Manikganj District , Rajbari District , Faridpur District and Tangail District . [30] In Bangladesh there were further outbreaks in subsequent years. [31] [7] September 1998 - May 1999 : in the states of Perak , Negeri Sembilan and Selangor in Malaysia . ... Hindustan Times . 27 May 2018 . Retrieved 28 May 2018 . ^ "After the outbreak" . ... Health and Science Bulletin . 8 (2): 6–11. Archived from the original on 28 September 2011. ^ "Arguments in Bahodderhat murder case begin" .
This is due to a hypothesised "meat factor" which enhances iron absorption. [27] Following are two tables showing the richest foods in heme and non-heme iron. [28] [ unreliable source? ] In both tables, food serving sizes may differ from the usual 100g quantity for relevancy reasons [ clarify ] . Arbitrarily, the guideline is set at 18 mg, which is the USDA Recommended Dietary Allowance for women aged between 19 and 50. [29] Abstract: richest foods in heme iron Food Serving size Iron % guideline clam [a] 100g 28 mg 155% pork liver 100g 18 mg 100% lamb kidney 100g 12 mg 69% cooked oyster 100g 12 mg 67% cuttlefish 100g 11 mg 60% lamb liver 100g 10 mg 57% octopus 100g 9.5 mg 53% mussel 100g 6.7 mg 37% beef liver 100g 6.5 mg 36% beef heart 100g 6.4 mg 35% Abstract: richest foods in non-heme iron Food Serving size Iron % guideline raw yellow beans 100g 7 mg 35% spirulina 15g 4.3 mg 24% falafel 140g 4.8 mg 24% soybean kernels 125ml=1/2cup 4.6 mg 23% spinach 125g 4.4 mg 22% lentil 125ml=1/2cup 3.5 mg 17.5% treacle (CSR Australia) 20ml=1Tbsp 3.4 mg 17% molasses (Bluelabel Australia) 20ml=1Tbsp 1.8 mg 9% candied ginger root 15g~3p 1.7 mg 8.5% toasted sesame seeds 10g 1.4 mg 7% cocoa (dry powder) 5g~1Tbsp .8 mg 4% Food recommendations for children [ edit ] Children at 6 months should start having solid food that contains enough iron, which could be found in both heme and non-heme iron [33] Heme iron : Red meat (for example, beef, pork, lamb, goat, or venison) Fatty fish Poultry (for example, chicken or turkey) Eggs Non-heme iron : Iron-fortified infant cereals Tofu Beans and lentils Dark green leafy vegetables Iron deficiency can have serious health consequences that diet may not be able to quickly correct; hence, an iron supplement is often necessary if the iron deficiency has become symptomatic. ... Archived from the original on 15 October 2014 . Retrieved 28 July 2014 . Lin, DM; Lin, ES; Tran, MH (October 2013).
Since 1973 the use of these drugs has been found to be associated with the development of tardive dyskinesia. [22] [23] Risk factors [ edit ] An increased risk of tardive dyskinesia has been associated with smoking in some studies, [24] [25] although a negative study does exist. [26] There seems to be a cigarette smoke-exposure-dependent risk for TD in people who are antipsychotic-treated . [27] Elderly peoples are also at a heightened risk for developing TD, [7] as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia. [19] TD is also more common in those that experience acute neurological side effects from antipsychotic drug treatment. [19] Racial discrepancies in TD rate also exist, with Africans and African Americans having higher rates of TD after exposure to antipsychotics. [7] Certain genetic risk factors for TD have been identified including polymorphisms in the genes encoding the D 3 , 5-HT 2A and 5-HT 2C receptors. [28] Prevention [ edit ] Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. ... NORD (National Organization for Rare Disorders) . 2015. Archived from the original on 28 August 2017 . Retrieved 11 June 2017 . ^ a b c d e f Vijayakumar, D; Jankovic, J (May 2016). ... "Smoking and tardive dyskinesia: lack of involvement of the CYP1A2 gene" . J Psychiatry Neurosci . 28 (3): 185–89. PMC 161742 . PMID 12790158 . ^ Zhang, XY; Yu, YQ; Sun, S; Zhang, X; Li, W; Xiu, MH; Chen da, C; Yang, FD; Zhu, F; Kosten, TA; Kosten, TR (August 2011).
Description Tardive dyskinesia is a debilitating motor disorder manifest as hyperkinetic, involuntary, repetitive movements predominantly of the orofacial region. It is a complication of treatment with so-called typical antipsychotic or neuroleptic agents, such as chlorpromazine or haloperidol, and is estimated to occur in 20 to 30% of chronic schizophrenics on long-term treatment (Thelma et al., 2008). Clinical Features In a review, Thelma et al. (2008) noted that age and African American ethnicity are both risk factors for the development of tardive dyskinesia. Inheritance Yassa and Ananth (1981) surveyed 500 inpatients receiving long-term neuroleptics and found 8 with first-degree relatives who were also on neuroleptics and suffering from a psychiatric disorder. All 8 proband-relative pairs were concordant for the presence or absence of tardive dyskinesia.
Annals of the New York Academy of Sciences . 1308 (1): 118–28. Bibcode : 2014NYASA1308..118N . doi : 10.1111/nyas.12330 . ... Annals of the New York Academy of Sciences . 1308 (1): 118–28. Bibcode : 2014NYASA1308..118N . doi : 10.1111/nyas.12330 .
Less common features included lid lag (21%), tongue myotonia (28%), and generalized hypertrophy (21%). ... Although many patients (43%) tried medication, only a few (28%) had relief. The most effective medications were mexiletine and carbamazepine, followed by phenytoin.
Paramyotonia congenita is a disorder that affects muscles used for movement (skeletal muscles). Beginning in infancy or early childhood, people with this condition experience bouts of sustained muscle tensing (myotonia) that prevent muscles from relaxing normally. Myotonia causes muscle stiffness that typically appears after exercise and can be induced by muscle cooling. This stiffness chiefly affects muscles in the face, neck, arms, and hands, although it can also affect muscles used for breathing and muscles in the lower body. Unlike many other forms of myotonia, the muscle stiffness associated with paramyotonia congenita tends to worsen with repeated movements.
Paramyotonia congenita of Von Eulenburg is characterised by exercise- or cold-induced myotonia and muscle weakness. Prevalence is unknown. The syndrome is nonprogressive and is transmitted as an autosomal dominant trait. It is caused by mutations in the gene encoding the alpha subunit of the type IV voltage-gated sodium channel (SCN4A; 17q23.3).
Paramyotonia congenita is an inherited condition that affects muscles used for movement ( skeletal muscles ), mainly in the face, neck, arms, and hands. Symptoms begin in infancy or early childhood and include episodes of sustained muscle tensing ( myotonia ) that prevent muscles from relaxing normally and lead to muscle weakness. Symptoms in paramyotonia congenita worsen during exposure to cold temperatures, and unlike many other forms of myotonia, worsen with exercise and repeated movements. This condition is caused by mutations in the SCN4A gene and is inherited in an autosomal dominant pattern.
