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| '''For patient information, click [[Creutzfeldt-Jakob disease (patient information)|here]]'''
| | __NOTOC__ |
| | {{Creutzfeldt-Jakob disease}} |
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| {{Infobox_Disease | | | {{CMG}}; {{AE}}, {{M.B}} |
| Name = {{PAGENAME}} |
| | ==[[Creutzfeldt-Jakob disease overview|Overview]]== |
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| Caption = |
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| DiseasesDB = 3166 |
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| ICD10 = {{ICD10|A|81|0|a|80}}, {{ICD10|F|02|1|f|00}} |
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| ICD9 = {{ICD9|046.1}} |
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| ICDO = |
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| OMIM = 123400 |
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| MedlinePlus = |
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| MeshID = D007562
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| }}
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| {{SI}}
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| {{CMG}}
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| ==Overview== | | ==[[Creutzfeldt-Jakob disease historical perspective|Historical Perspective]]== |
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| '''Creutzfeldt-Jakob disease''' ('''CJD''') is a very rare and incurable [[degeneration (medical)|degenerative]] [[neurology|neurological disorder]] ([[brain]] [[disease]]) that is ultimately fatal. Among the types of [[transmissible spongiform encephalopathy]] found in humans, it is the most common.
| | ==[[Creutzfeldt-Jakob disease classification|Classification]]== |
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| ==Historical Perspective== | | ==[[Creutzfeldt-Jakob disease pathophysiology|Pathophysiology]]== |
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| The disease was first described by two German [[neurologist]]s, [[Hans Gerhard Creutzfeldt]] and [[Alfons Maria Jakob]]. Some of the clinical findings described in their first papers do not match current criteria for Creutzfeldt-Jakob disease, and it is considered highly likely that at least two of the patients in initial studies were suffering from a different disorder.
| | ==[[Creutzfeldt-Jakob disease causes|Causes]]== |
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| [[Stanley B. Prusiner]] was awarded the [[Nobel Prize in physiology or medicine]] in 1997 for his discovery of [[prion]]s. For more than a decade, [[Yale University]] [[neuropathologist]] [[Laura Manuelidis]] has been challenging this explanation for the disease. In January 2007 she and her colleagues published an article in the ''[[Proceedings of the National Academy of Science]]'' and reported that they have found a [[virus]]-like particle (but without finding [[nucleic acid]]s so far) in less than 10% of the cells a scrapie-infected cell line and in a mouse cell line infected by a human CJD agent.<ref name="Manuelidis2007">{{cite journal| author=Manuelidis L| coauthors=Yu ZX, Barquero N, Mullins B|date=February 6, 2007| title=Cells infected with scrapie and Creutzfeldt-Jakob disease agents produce intracellular 25-nm virus-like particles| journal=Proceedings of the National Academy of Science| volume=104| issue=6| pages=1975-1970| pmid=17267596| url=http://www.pnas.org/cgi/content/full/104/6/1965| accessdate=2007-09-24}}</ref> | | ==[[Creutzfeldt-Jakob disease differential diagnosis|Differentiating Creutzfeldt-Jakob disease from other Diseases]]== |
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| ==Classification== | | ==[[Creutzfeldt-Jakob disease epidemiology and demographics|Epidemiology and Demographics]]== |
| The prion that is believed to cause Creutzfeldt-Jakob exhibits at least two stable conformations. One, the native state, is water-soluble and present in healthy cells. As of 2006, its biological function is unknown. The other conformational state is very poorly water-soluble and readily forms protein aggregates.
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| There are two typed CJD, classic and variant form. Classic CJD characteristics, as compared to variant CJD, are presented in the table below.
| | ==[[Creutzfeldt-Jakob disease risk factors|Risk Factors]]== |
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| Transmissible spongiform encephalopathy diseases are caused by prions. The diseases are thus sometimes called prion diseases.
| | ==[[Creutzfeldt-Jakob disease screening|Screening]]== |
| Other prion diseases include [[Gerstmann-Sträussler-Scheinker syndrome]] ([[GSS]]), [[fatal familial insomnia]] (FFI) and [[kuru]] in humans, as well as [[bovine spongiform encephalopathy]] ([[BSE]]) commonly known as [[mad cow disease]], [[chronic wasting disease]] ([[CWD]]), and scrapie in sheep.
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| ==Pathophysiology== | | ==[[Creutzfeldt-Jakob disease natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| The CJD prion is dangerous because it promotes refolding of native proteins into the diseased state. The number of misfolded [[protein]] molecules will increase exponentially, and the process leads to a large quantity of insoluble prions in affected cells. This mass of misfolded [[protein]]s disrupts cell function and causes cell death. Once the prion is transmitted, the defective proteins invade the brain and are produced in a self-sustaining feedback loop, causing exponential spread of the prion, death within a few months, although a few patients have been known to live as long as two years.
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| == Epidemiology and Demographics ==
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| Classic [[CJD]] has been recognized since the early 1920s. The most common form of classic [[CJD]] is believed to occur sporadically, caused by the spontaneous transformation of normal prion proteins into abnormal prions.
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| *This sporadic disease occurs worldwide, including the United States, at a rate of approximately one case per 1 million population per year, although rates of up to two cases per million are not unusual.
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| *The risk of [[CJD]] increases with age, and in persons aged over 50 years of age, the annual rate is approximately 3.4 cases per million.
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| *In recent years, the United States has reported fewer than 300 cases of [[CJD]] a year.
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| Whereas the majority of cases of [[CJD]] (about 85%) occur as sporadic disease, a smaller proportion of patients (5-15%) develop CJD because of inherited mutations of the prion [[protein]] gene. These inherited forms include [[Gerstmann-Straussler-Scheinker syndrome]] and [[fatal familial insomnia]].
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| [[Image:Figure annual deaths 2004.png|left|thumb|300px|CJD deaths and age-adjusted death rate, USA, 1979-2004]]
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| ===Incidence and prevalence===
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| Although CJD is the most common human [[prion]] disease, it is still rare and only occurs in about one out of every one million people. It usually affects people aged 45–75, most commonly appearing in people between the ages of 60–65. The exception to this is the more recently-recognised 'variant' CJD (vCJD), which occurs in younger people.
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| [[Centers for Disease Control and Prevention|CDC]] monitors the occurrence of CJD in the United States through periodic reviews of national mortality data: According to the CDC:
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| * CJD occurs worldwide at a rate of about 1 case per million population per year.
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| * On the basis of mortality surveillance from 1979 to 1994, the annual [[incidence (epidemiology)|incidence]] of CJD remained stable at approximately 1 case per [[million]] persons in the United States.
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| * In the United States, CJD deaths among persons younger than 30 years of age are extremely rare (fewer than 5 deaths per [[1000000000 (number)|billion]] per year).
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| * The disease is found most frequently in patients 55–65 years of age, but cases can occur in persons older than 90 years and younger than 55 years of age.
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| * In more than 85% of cases, the duration of CJD is less than 1 year (median: 4 months) after onset of symptoms.<ref name="titleHomepage | CDC Classic CJD">{{cite web |url=http://www.cdc.gov/ncidod/dvrd/cjd/index.htm |title=Homepage | CDC Classic CJD |accessdate=2007-12-02 |format= |work=}}</ref><ref name="titleVariant CJD, Fact Sheet | CDC vCJD">{{cite web |url=http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm |title=Variant CJD, Fact Sheet | CDC vCJD |accessdate=2007-12-02 |format= |work=}}</ref>
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| ===New concerns on incidence and prevalence===
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| In ''[[The Lancet]]'' (June 2006), a University College London team suggested that it may take more than 50 years for vCJD to develop, from their studies of [[kuru (disease)|kuru]], a similar disease in [[Papua New Guinea]].<ref name="titleForbes.com">{{cite web |url=http://www.forbes.com/forbeslife/health/feeds/hscout/2006/06/22/hscout533415.html |title=forbeslife |accessdate=2007-12-02 |format= |work=}}</ref> The reasoning behind the claim is that kuru was transmitted through [[cannibalism]] in [[Papua New Guinea]] when relatives would eat their dead relative's bodies as a sign of [[mourning]]. In the 1950s, the practice was banned, thereby preventing any further possible transmission. In the late 20th century, however, kuru reached epidemic proportions in certain Papua New Guinean communities, therefore suggesting that vCJD may also have a similar [[incubation period]] of 30 to 50 years. A critique to this theory is that while mortuary cannibalism was banned in Papua New Guinea in the 1950s, that does not necessarily mean that the practice ended. Fifteen years later [[Jared Diamond]] was informed by Papuans that the practice continued.<ref>{{cite web|url=http://www..nature.com/nature/journal/v407/n6800/full/407025a0.html|title=Diamond, J.M. (2000)"Archaeology: Talk of cannibalism" ''Nature'' 407, 25-26<!--INSERT TITLE-->}}</ref>
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| These researchers noticed a genetic variation in some kuru patients that has been known to promote long [[incubation period]]s. They have also proposed that individuals who contracted CJD in the early 1990s represent a distinct genetic subpopulation, with unusually short incubation periods for BSE. This means that there may be many more vCJD patients who have longer incubation periods, which may surface many years later.<ref name="titleForbes.com">{{cite web |url=http://www.forbes.com/forbeslife/health/feeds/hscout/2006/06/22/hscout533415.html |title=forbeslife |accessdate=2007-12-02 |format= |work=}}</ref>
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| ==Symptoms==
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| <!--
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| [[Image:http://pathology.mc.duke.edu/neuropath/CNSlecture2/cjd.jpg]] The spongiform look of the cortex cross-section is characteristic of CJD. -->
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| The first [[symptom]] of CJD is rapidly progressive [[dementia]], leading to [[memory]] loss, [[personality]] changes and [[hallucinations]]. This is accompanied by physical problems such as [[Speech communication|speech]] impairment, jerky movements ([[myoclonus]]), balance and coordination dysfunction ([[ataxia]]), changes in [[gait (human)|gait]], rigid [[posture]], and [[seizures]]. The duration of the disease varies greatly, but sporadic (non-inherited) CJD can be fatal within months or even weeks (Johnson, 1998). In some people, the symptoms can continue for years. In most patients, these symptoms are followed by involuntary movements and the appearance of a typical diagnostic [[electroencephalogram]] tracing.
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| The symptoms of CJD are caused by the progressive [[cell death|death]] of the brain's [[neuron|nerve cells]], which is associated with the build-up of abnormal [[prion]] [[proteins]]. When brain tissue from a CJD patient is examined under a [[microscope]], many tiny holes can be seen where whole areas of nerve cells have died. The word 'spongiform' in '[[transmissible spongiform encephalopathies]]' refers to the 'spongy' appearance of the [[brain]] tissue.
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| ==Diagnosis== | | ==Diagnosis== |
| The diagnosis of CJD is suspected when there are typical clinical symptoms and signs such as rapidly progressing dementia with [[myoclonus]]. Further investigation can then be performed to support the diagnosis including
| | [[Creutzfeldt-Jakob disease diagnostic study of choice|Diagnostic study of choice]] | [[Creutzfeldt-Jakob disease history and symptoms|History and Symptoms]] | [[Creutzfeldt-Jakob disease physical examination|Physical Examination]] | [[Creutzfeldt-Jakob disease laboratory findings|Laboratory Findings]] | [[Creutzfeldt-Jakob disease electrocardiogram|Electrocardiogram]] | [[Creutzfeldt-Jakob disease x ray|X-Ray Findings]] | [[Creutzfeldt-Jakob disease echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Creutzfeldt-Jakob disease CT scan|CT-Scan Findings]] | [[Creutzfeldt-Jakob disease MRI|MRI Findings]] | [[Creutzfeldt-Jakob disease other imaging findings|Other Imaging Findings]] | [[Creutzfeldt-Jakob disease other diagnostic studies|Other Diagnostic Studies]] |
| * [[Electroencephalography]] — often has characteristic triphasic spikes
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| * [[Cerebrospinal fluid]] analysis for [[14-3-3 protein]]
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| * [[MRI]] of the brain — often shows high signal intensity in the caudate nucleus and putamen bilaterally on T2-weighted images.
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| Diffusion Weighted Imaging (DWI) images are the most sensitive. In about 24% of cases DWI shows only cortical hyperintensity; in 68%, cortical and subcortical abnormalities; and in 5%, only subcortical anomalies.<ref>{{cite journal|last= Young|first= Geoffrey S.|coauthors= Michael D. Geschwind, Nancy J. Fischbein, Jennifer L. Martindale, Roland G. Henry, Songling Liu, Ying Lu, Stephen Wong, Hong Liu, Bruce L. Miller and William P. Dillon|title=Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Imaging in Creutzfeldt-Jakob Disease: High Sensitivity and Specificity for Diagnosis|journal=American Journal of Neuroradiology|volume= 26|pages=1551-1562|date=June-July 2005|publisher=American Society of Neuroradiology|url=http://www.ajnr.org/cgi/content/full/26/6/1551| accessdate = 2007-10-30}}</ref>
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| The involvement of the thalamus can be found in sCJD, even is stronger and constant in vCJD.<ref>{{cite journal | last =Tschampa | first =Henriette J. | authorlink = | coauthors =Petra Mürtz, Sebastian Flacke, Sebastian Paus, Hans H. Schild and Horst Urbach | title =Thalamic Involvement in Sporadic Creutzfeldt-Jakob Disease: A Diffusion-Weighted MR Imaging Study | journal =American Journal of Neuroradiology | volume =24 | pages =908-915 | publisher =American Society of Neuroradiology |date=May 2003 | url =http://www.ajnr.org/cgi/content/full/24/5/908 | accessdate = 2007-10-30}}</ref>
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| In one third of patients with sporadic CJD, deposits of "prion protein (scrapie)," [[PrpSc|PrP<SUP>Sc</SUP>]], can be found in the skeletal muscle and/or the spleen. Diagnosis of vCJD can be supported by biopsy of the tonsils, which harbour significant amounts of PrpSc; however, [[biopsy]] of brain tissue is the definitive diagnostic test.
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| *Clinical and Pathologic Characteristics:<ref>{{cite journal |author=Belay ED, Schonberger LB |title=Variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy |journal=Clin. Lab. Med. |volume=22 |issue=4 |pages=849-62, v-vi |year=2002 |pmid=12489284 |doi=}}</ref>
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| <table border="0" width="80%" id="table1" class="wikitable">
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| <tr>
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| <td>Characteristic </td>
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| <td>Classic CJD</td>
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| <td>Variant CJD</td>
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| </tr>
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| <tr>
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| <td>Median age at death</td>
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| <td>68 years</td>
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| <td>28 years </td>
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| </tr>
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| <tr>
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| <td>Median duration of illness</td>
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| <td>4-5 months</td>
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| <td>13-14 months </td>
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| </tr>
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| <tr>
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| <td>Clinical signs and symptoms</td>
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| <td>Dementia; early neurologic signs</td>
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| <td>Prominent psychiatric/behavioral symptoms; painful [[dysesthesias]];
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| delayed neurologic signs </td>
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| </tr>
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| <tr>
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| <td>Periodic sharp waves on [[electroencephalogram]]</td>
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| <td>Often present</td>
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| <td>Often absent</td>
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| </tr>
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| <tr>
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| <td>Signal hyperintensity in the [[caudate nucleus]] and [[putamen]] on diffusion-weighted and FLAIR MRI</td>
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| <td>Often present</td>
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| <td>Often absent</td>
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| </tr>
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| <tr>
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| <td>"[[Pulvinar]] sign" on MRI</td>
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| <td>Not reported</td>
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| <td>Present in >75% of cases</td>
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| </tr>
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| <tr>
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| <td>[[Immunohistochemical staining|Immunohistochemical analysis]] of brain tissue</td>
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| <td>Variable accumulation.</td>
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| <td>Marked accumulation of protease-resistant prion protein</td>
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| </tr>
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| <tr>
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| <td>Presence of agent in [[lymphoid]] tissue</td>
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| <td>Not readily detected</td>
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| <td>Readily detected </td>
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| </tr>
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| <tr>
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| <td>Increased [[glycoform]] ratio on immunoblot analysis of
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| protease-resistant prion protein</td>
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| <td>Not reported </td>
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| <td>Marked accumulation of protease-resistant prion protein </td>
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| <tr>
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| <td>Presence of amyloid plaques in brain tissue</td>
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| <td>May be present</td>
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| <td>May be present</td>
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| </tr>
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| </table>
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| *An abnormal signal in the posterior thalami on T2- and diffusion-weighted images and fluid-attenuated inversion recovery sequences on brain magnetic resonance imaging (MRI); in the appropriate clinical context, this signal is highly specific for vCJD. (Source: CDC)
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| ==Treatment== | | ==Treatment== |
| | [[Creutzfeldt-Jakob disease medical therapy|Medical Therapy]] | [[Creutzfeldt-Jakob disease interventions|Interventions]] | [[Creutzfeldt-Jakob disease surgery|Surgery]] | [[Creutzfeldt-Jakob disease primary prevention|Primary Prevention]] | [[Creutzfeldt-Jakob disease secondary prevention|Secondary Prevention]] | [[Creutzfeldt-Jakob disease cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Creutzfeldt-Jakob disease future or investigational therapies|Future or Investigational Therapies]] |
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| As of 2007, there is no cure for CJD, a fatal disease, and the search for viable treatments continues. An experimental treatment was given to a Northern Irish teenager, [[Jonathan Simms]], beginning in January 2003.<ref>{{cite web | title =Teenager with vCJD 'stable'' | publisher = BBC News | date = [[13 December]] [[2004]] | url = http://news.bbc.co.uk/2/hi/uk_news/northern_ireland/4092363.stm | accessdate = 2007-01-01 }}</ref> The medication, called [[pentosan polysulphate]] (PPS) and used to treat [[interstitial cystitis]], is infused into the patient's [[ventricular system|lateral ventricle]] within the brain. PPS does not seem to stop the disease from progressing, and both brain function and tissue continue to be lost. However, the treatment is alleged to slow the progression of the otherwise untreatable disease, and may have contributed to the longer than expected survival of the seven patients that were studied.<ref>{{cite web
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| | last = Bone | first = Ian | title =Intraventricular Pentosan Polysulphate in Human Prion Diseases: A study of Experience in the United Kingdom | publisher = Medical Research Council | date = [[12 July]] [[2006]] | url = http://www.mrc.ac.uk/NewsViewsAndEvents/News/MRC001707 | accessdate = 2007-01-01 }}</ref> The CJD Therapy Advisory Group to the UK Health Departments advises that data are not sufficient to support claims that [[pentosan polysulphate]] is an effective treatment and suggests that further research in animal models is appropriate.<ref>{{cite web|title=Use of Pentosan Polysulphate in the treatment of, or prevention of, vCJD|url = http://www.dh.gov.uk/en/Policyandguidance/Healthandsocialcaretopics/CJD/CJDgeneralinformation/DH_4031039|publisher= Department of Health:CJD Therapy Advisory Group| accessdate = 2007-10-30}}</ref> A 2007 review of the treatment of 26 patients with PPS finds no proof of efficacy because of the lack of accepted objective criteria.<ref>{{cite journal |author=Rainov NG, Tsuboi Y, Krolak-Salmon P, Vighetto A, Doh-Ura K |title=Experimental treatments for human transmissible spongiform encephalopathies: is there a role for pentosan polysulfate? |journal=Expert opinion on biological therapy |volume=7 |issue=5 |pages=713-26 |year=2007 |pmid=17477808 |doi=10.1517/14712598.7.5.713}}</ref>
| | [[Creutzfeldt-Jakob disease case study one|Case #1]] |
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| Scientists have investigated using [[RNA interference]] to slow the progression of [[scrapie]] in mice. The RNA blocks production of the protein that the CJD process transforms into [[prion]]s. This research is unlikely to lead to a human therapy for many years.<ref>{{cite web | title =Revamp of brain 'could slow CJD' | publisher = BBC News | date = [[4 December]] [[2006]] | url = http://news.bbc.co.uk/2/hi/health/6198072.stm | accessdate = 2007-01-01 }}</ref>
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| ==Transmission==
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| The defective protein can be transmitted by [[human growth hormone]] (hGH) products, [[cornea]]l grafts, dural grafts or [[electrode]] implants (acquired or [[Iatrogenesis|iatrogenic]] form: iCJD); it can be inherited (hereditary or familial form: fCJD); or it may appear for the first time in the patient (sporadic form: sCJD). In the hereditary form, a [[mutation]] occurs in the [[gene]] for PrP, [[PRNP]]. 10 to 15% of CJD cases are inherited. (CDC)
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| The disease has also been shown to result from usage of [[Human growth hormone|HGH]] drawn from the [[pituitary gland]]s of [[cadaver]]s who died from Creutzfeldt-Jakob Disease,<ref name="titleHGH Linked to Brain Eater">{{cite web |url=http://www.wired.com/news/medtech/0,1286,62998,00.html |title=HGH Linked to Brain Eater |accessdate=2007-12-02 |format= |work=}}</ref> though the known incidence of this cause is (as of April 2004) quite small. The risk of infection through cadaveric HGH usage in the US only ceased when the medication was withdrawn in 1985.
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| It is thought that humans can contract the disease by consuming material from animals infected with the bovine form of the disease. The only suspected cases to arise thus far have been vCJD, although there are fears — based on animal studies — that consuming beef or beef products containing [[prion]] particles can also cause the development of classic CJD.
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| [[Cannibalism]] has also been implicated as a transmission mechanism for abnormal [[prion]]s, causing the disease known as [[Kuru (disease)|kuru]], found primarily among women and children of the [[Fore Tribe|Fore tribe]] in [[Papua New Guinea]]. While the men of the tribe ate the body of the deceased and were not affected, the women and children ate the brain and contracted the disease from infected brain tissue.
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| [[Prion]]s, the [[infectious agent]] of CJD, may not be inactivated by means of routine [[surgical instrument]] [[Autoclave|sterilization]] procedures. The [[World Health Organization]] and the US [[Centers for Disease Control and Prevention]] recommend that heat and chemical decontamination be used in combination to process instruments that come in contact with high-infectivity tissues. No cases of [[iatrogenic]] transmission of CJD have been reported subsequent to the adoption of current sterilization procedures, or since 1976.<ref>{{cite web|title =Questions and Answers: Creutzfeldt-Jakob Disease Infection-Control Practices|work =Infection Control Practices/CJD (Creutzfeldt-Jakob Disease, Classic)|publisher =Centers for Disease Control and Prevention|date =[[January 4]] [[2007]]|url = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm#sterilization|accessdate = 2007-06-09}}</ref><ref>{{cite web|title =WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies|Publisher =World Health Organization: Communicable Disease Surveillance and Control|date =[[26 March]] [[1999]]|url =http://www.who.int/csr/resources/publications/bse/WHO_CDS_CSR_APH_2000_3/en/|accessdate = 2007-06-09}}</ref><ref>{{cite journal | author=McDonnell G, Burke P. | title=The challenge of prion decontamination | journal=Clin Infect Dis | year=2003 | volume=36 | pages=1152–4 }}</ref> [[Copper]]-[[hydrogen peroxide]] has been suggested as an alternative to the current recommendation of [[sodium hydroxide]] or [[sodium hypochlorite]].<ref>{{cite journal | author=Solassol J, Pastore M, Crozet C, ''et al.'' | title=A novel copper-hydrogen peroxide formulation for prion decontamination | journal=J Infect Dis | year=2006 | volume=194 | pages=865–869 }}</ref> [[Thermal depolymerization]] also destroys [[prion]]s in infected organic and inorganic matter, since the process dissolves protein at the molecular level.
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| ==Blood donor restrictions==
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| In 2004 a new report published in the ''[[The Lancet|Lancet]]'' medical journal showed that vCJD can be transmitted by [[blood transfusion]]s.<ref name="pmid15302196">{{cite journal |author=Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW |title=Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient |journal=Lancet |volume=364 |issue=9433 |pages=527–9 |year=2004 |pmid=15302196 |doi=10.1016/S0140-6736(04)16811-6}}</ref> The finding alarmed healthcare officials because a large [[epidemic]] of the disease might arise in the near future. There is no test to determine if a [[blood donor]] is [[infected]] and in the latent phase of vCJD. In reaction to this report, the [[British government]] banned anyone who had received a [[blood transfusion]] since January 1980 from donating blood.
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| On [[May 28]], [[2002]], the [[United States]] [[Food and Drug Administration]] instituted a policy that excludes from donation anyone who spent at least 6 months in certain Western European countries, (or 3 months in the United Kingdom), from 1980 to 1996. Given the large number of U.S. military personnel and their dependents residing in Europe, it was expected that over 7% of donors would be deferred due to the policy. Later changes to this policy have relaxed the restriction to a cumulative total of 5 years or more of civilian travel in Western European countries (6 months or more if military). The 3-month restriction on travel to the UK, however, has not been changed.<ref name="titleIn-Depth Discussion of Variant Creutzfeld-Jacob Disease and Blood Donation">{{cite web |url=http://www.redcross.org/services/biomed/blood/supply/cjdv.html |title=In-Depth Discussion of Variant Creutzfeld-Jacob Disease and Blood Donation |accessdate=2007-12-02 |format= |work=}}</ref>
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| A similar policy applies to potential donors to the [[Australian Red Cross]]' [[Australian Red Cross Blood Service|Blood Service]], precluding people who have spent a cumulative time of six months or more in the [[United Kingdom]] between 1980 and 1996.
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| The [[Singapore Red Cross]] precludes potential donors who have spent a cumulative time of three months or more in the [[United Kingdom]] between 1980 and 1996.
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| As of 1999, [[Health Canada]] announced a policy to defer individuals from donating blood if they have lived within the [[United Kingdom]] for one month or more from Jan. 1, 1980 to Dec. 31, 1996. In 2000, the same policy was applied to people who have resided in [[France]], for at least three months from Jan. 1980 to Dec. 1996. [[Canada]] will not accept blood from a person who has spent more than 6 months in a Western European country since January 1, 1980.<ref name="titleH�ma-Qu�bec, blood, donors, blood donation, volunteers, receivers, blood drives, Globule, blood clinics, stem cells, blood cord, human tissues, safety, H�ma-Qu�bec, job openings, press center">{{cite web |url=http://www.hema-quebec.qc.ca/anglais/dondesang/qualifidonneurs.htm |title=H�ma-Qu�bec, blood, donors, blood donation, volunteers, receivers, blood drives, Globule, blood clinics, stem cells, blood cord, human tissues, safety, H�ma-Qu�bec, job openings, press center |accessdate=2007-12-02 |format= |work=}}</ref>
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| The [http://www.bloddonor.dk/ Association of Blooddonors] of Denmark precludes potential donors who have spent a cumulative time of at least twelve months in the [[United Kingdom]] between 1 January 1980 and 31 December 1996.
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| The Swiss [http://redcross.ch/org/institutions/blood/index-de.php Blutspendedienst SRK] precludes potential donors who have spent a cumulative time of at least six months in the [[United Kingdom]] between 1 January 1980 and 31 December 1996.
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| ==References==
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| {{reflist|2}}
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| {{Prion diseases}}
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| {{Mental and behavioural disorders}}
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| {{SIB}}
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| {{Link FA|es}}
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| [[ca:Malaltia de Creutzfeldt-Jakob]]
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| [[cs:Creutzfeldt-Jakobova nemoc]]
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| [[da:CJD]]
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| [[de:Creutzfeldt-Jakob-Krankheit]]
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| [[es:Enfermedad de Creutzfeldt-Jakob]]
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| [[fr:Maladie de Creutzfeldt-Jakob]]
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| [[hr:Creutzfeldt-Jakobova bolest]]
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| [[id:Penyakit Creutzfeldt-Jakob]]
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| [[it:Malattia di Creutzfeldt-Jakob]]
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| [[he:מחלת קרויצפלד-יעקב]]
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| [[hu:Creutzfeldt–Jakob-szindróma]]
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| [[nl:Ziekte van Creutzfeldt-Jakob]]
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| [[ja:クロイツフェルト・ヤコブ病]]
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| [[no:Creutzfeldt-Jakobs sykdom]]
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| [[pl:Choroba Creutzfeldta-Jakoba]]
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| [[pt:Doença de Creutzfeldt-Jakob]]
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| [[ru:Болезнь Крейтцфельдта — Якоба]]
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| [[sh:Creutzfeldt-Jakobova bolest]]
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| [[fi:Creutzfeldt–Jakobin tauti]]
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| [[sv:Creutzfeldt–Jakobs sjukdom]]
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| [[zh:克雅二氏病]]
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| {{WH}}
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| {{WS}}
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| [[Category:Overview complete]] | | [[Category: (name of the system)]] |
| [[Category:Neurology]]
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| [[Category:Disease]]
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| [[Category:Transmissible spongiform encephalopathies]]
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