Parkinson's disease differential diagnosis: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
 
(23 intermediate revisions by 3 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Parkinson's disease}}
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Parkinson%27s_disease]]


Please help WikiDoc by adding more content here.  It's easy!  Click  [[Help:How_to_Edit_a_Page|here]]  to learn about editing.
{{CMG}}; {{AE}} {{Fs}}


==Overview==
==Overview==
Parkinson disease must be differentiated from other diseases that can mimic this disease [[Clinical|clinically]] or [[Radiological|radiologically]] such as: essential tremor, scans without evidence of dopaminergic deficit (SWEDD), dementia with Lewy bodies, multiple system atrophy, corticobasal degeneration, progressive supranuclear palsy, idiopathic and familial basal ganglia calcification, and secondary parkinsonism.


==Differential Diagnosis==
==Differential Diagnosis==


Parkinson disease must be differentiated from other diseases that can mimic this disease [[Clinical|clinically]] or [[Radiological|radiologically]] such as:
*Parkinson disease must be differentiated from other diseases that can mimic this disease [[Clinical|clinically]] or [[Radiological|radiologically]] such as:
===Essential tremor===
*[[Essential tremor]] is demonstrated by bilateral resting tremor of arms, [[head]], [[chin]] and [[trunk]]. [[Tremor]] of [[Parkinson's disease|PD]] is action tremor and it seems to be easy to differentiate it from resting tremor of [[Essential tremor|ET]] but sometimes we can see resting tremor in [[Parkinson's disease|PD]] patient and conversely action tremor in [[Essential tremor|ET]] patients.<ref name="pmid10519872">{{cite journal |vauthors=Jankovic J, Schwartz KS, Ondo W |title=Re-emergent tremor of Parkinson's disease |journal=J. Neurol. Neurosurg. Psychiatry |volume=67 |issue=5 |pages=646–50 |date=November 1999 |pmid=10519872 |pmc=1736624 |doi= |url=}}</ref><ref name="pmid11594921">{{cite journal |vauthors=Louis ED, Levy G, Côte LJ, Mejia H, Fahn S, Marder K |title=Clinical correlates of action tremor in Parkinson disease |journal=Arch. Neurol. |volume=58 |issue=10 |pages=1630–4 |date=October 2001 |pmid=11594921 |doi= |url=}}</ref>
===Scans without evidence of dopaminergic deficit (SWEDD)===
*Patients with scans without evidence of dopaminergic deficit have [[upper extremity]] resting [[tremor]] but their disease does not progress to the complete [[Parkinson's disease|PD]] and there are no evidence of [[dopamine]] depletion in their [[Nigrostriatal pathway|NS]].<ref name="pmid17712858">{{cite journal |vauthors=Schneider SA, Edwards MJ, Mir P, Cordivari C, Hooker J, Dickson J, Quinn N, Bhatia KP |title=Patients with adult-onset dystonic tremor resembling parkinsonian tremor have scans without evidence of dopaminergic deficit (SWEDDs) |journal=Mov. Disord. |volume=22 |issue=15 |pages=2210–5 |date=November 2007 |pmid=17712858 |doi=10.1002/mds.21685 |url=}}</ref>
===Dementia with Lewy bodies===
*[[Dementia]] will finally occurs in the most cases of [[Parkinson's disease|Parkinson disease]] but the timing of [[dementia]] in [[Parkinson's disease|PD]] is after full developing of [[Parkinson's disease|PD]] and mostly after at least one year of disease start date. When [[dementia]] occurs with or before the [[signs]] and [[symptoms]] of [[Parkinson's disease|Parkinson disease]] we will categorize it as [[Dementia With Lewy Bodies|dementia with lewy body]].<ref name="pmid28592453">{{cite journal |vauthors=McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems J, Ballard CG, Bayston A, Beach TG, Blanc F, Bohnen N, Bonanni L, Bras J, Brundin P, Burn D, Chen-Plotkin A, Duda JE, El-Agnaf O, Feldman H, Ferman TJ, Ffytche D, Fujishiro H, Galasko D, Goldman JG, Gomperts SN, Graff-Radford NR, Honig LS, Iranzo A, Kantarci K, Kaufer D, Kukull W, Lee VMY, Leverenz JB, Lewis S, Lippa C, Lunde A, Masellis M, Masliah E, McLean P, Mollenhauer B, Montine TJ, Moreno E, Mori E, Murray M, O'Brien JT, Orimo S, Postuma RB, Ramaswamy S, Ross OA, Salmon DP, Singleton A, Taylor A, Thomas A, Tiraboschi P, Toledo JB, Trojanowski JQ, Tsuang D, Walker Z, Yamada M, Kosaka K |title=Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium |journal=Neurology |volume=89 |issue=1 |pages=88–100 |date=July 2017 |pmid=28592453 |pmc=5496518 |doi=10.1212/WNL.0000000000004058 |url=}}</ref><ref name="pmid27492190">{{cite journal |vauthors=Boeve BF, Dickson DW, Duda JE, Ferman TJ, Galasko DR, Galvin JE, Goldman JG, Growdon JH, Hurtig HI, Kaufer DI, Kantarci K, Leverenz JB, Lippa CF, Lopez OL, McKeith IG, Singleton AB, Taylor A, Tsuang D, Weintraub D, Zabetian CP |title=Arguing against the proposed definition changes of PD |journal=Mov. Disord. |volume=31 |issue=11 |pages=1619–1622 |date=November 2016 |pmid=27492190 |pmc=5168716 |doi=10.1002/mds.26721 |url=}}</ref>
===Multiple system atrophy===
*[[Multiple system atrophy|MSA]] is an [[idiopathic]] disease<ref name="pmid18825660">{{cite journal |vauthors=Wenning GK, Stefanova N, Jellinger KA, Poewe W, Schlossmacher MG |title=Multiple system atrophy: a primary oligodendrogliopathy |journal=Ann. Neurol. |volume=64 |issue=3 |pages=239–46 |date=September 2008 |pmid=18825660 |doi=10.1002/ana.21465 |url=}}</ref> characterized by [[Autonomic nervous system|autonomic]] problems such as [[urogenital]] dysfunction, [[ataxia]] and [[parkinsonism]] [[symptoms]].<ref name="pmid19909915">{{cite journal |vauthors=Stefanova N, Bücke P, Duerr S, Wenning GK |title=Multiple system atrophy: an update |journal=Lancet Neurol |volume=8 |issue=12 |pages=1172–8 |date=December 2009 |pmid=19909915 |doi=10.1016/S1474-4422(09)70288-1 |url=}}</ref> [[Multiple system atrophy|MSA]] patients have resting [[tremor]] in arms, rigidity and [[bradykinesia]].<ref name="pmid16049636">{{cite journal |vauthors=Geser F, Seppi K, Stampfer-Kountchev M, Köllensperger M, Diem A, Ndayisaba JP, Ostergaard K, Dupont E, Cardozo A, Tolosa E, Abele M, Dodel R, Klockgether T, Ghorayeb I, Yekhlef F, Tison F, Daniels C, Kopper F, Deuschl G, Coelho M, Ferreira J, Rosa MM, Sampaio C, Bozi M, Schrag A, Hooker J, Kim H, Scaravilli T, Mathias CJ, Fowler C, Wood N, Quinn N, Widner H, Nilsson CF, Lindvall O, Schimke N, Eggert KM, Oertel W, del Sorbo F, Carella F, Albanese A, Pellecchia MT, Barone P, Djaldetti R, Meco G, Colosimo C, Gonzalez-Mandly A, Berciano J, Gurevich T, Giladi N, Galitzky M, Ory F, Rascol O, Kamm C, Buerk K, Maass S, Gasser T, Poewe W, Wenning GK |title=The European Multiple System Atrophy-Study Group (EMSA-SG) |journal=J Neural Transm (Vienna) |volume=112 |issue=12 |pages=1677–86 |date=December 2005 |pmid=16049636 |doi=10.1007/s00702-005-0328-y |url=}}</ref> The underlying [[pathophysiology]] of [[Multiple system atrophy|MSA]] is [[myelin]] dysfunction and [[inclusions]] in [[glial cell]] throughout [[CNS]].<ref name="pmid18825660">{{cite journal |vauthors=Wenning GK, Stefanova N, Jellinger KA, Poewe W, Schlossmacher MG |title=Multiple system atrophy: a primary oligodendrogliopathy |journal=Ann. Neurol. |volume=64 |issue=3 |pages=239–46 |date=September 2008 |pmid=18825660 |doi=10.1002/ana.21465 |url=}}</ref><ref name="pmid9736024">{{cite journal |vauthors=Matsuo A, Akiguchi I, Lee GC, McGeer EG, McGeer PL, Kimura J |title=Myelin degeneration in multiple system atrophy detected by unique antibodies |journal=Am. J. Pathol. |volume=153 |issue=3 |pages=735–44 |date=September 1998 |pmid=9736024 |pmc=1853025 |doi=10.1016/S0002-9440(10)65617-9 |url=}}</ref>
===Corticobasal degeneration===
*Clinical features of [[Corticobasal degeneration|CBD]] is asymmetric movement disorders including rigidity, [[akinesia]] and [[dystonia]].<ref name="pmid5634369">{{cite journal |vauthors=Rebeiz JJ, Kolodny EH, Richardson EP |title=Corticodentatonigral degeneration with neuronal achromasia |journal=Arch. Neurol. |volume=18 |issue=1 |pages=20–33 |date=January 1968 |pmid=5634369 |doi= |url=}}</ref><ref name="pmid9489528">{{cite journal |vauthors=Wenning GK, Litvan I, Jankovic J, Granata R, Mangone CA, McKee A, Poewe W, Jellinger K, Ray Chaudhuri K, D'Olhaberriague L, Pearce RK |title=Natural history and survival of 14 patients with corticobasal degeneration confirmed at postmortem examination |journal=J. Neurol. Neurosurg. Psychiatry |volume=64 |issue=2 |pages=184–9 |date=February 1998 |pmid=9489528 |pmc=2169933 |doi= |url=}}</ref><ref name="pmid2381527">{{cite journal |vauthors=Riley DE, Lang AE, Lewis A, Resch L, Ashby P, Hornykiewicz O, Black S |title=Cortical-basal ganglionic degeneration |journal=Neurology |volume=40 |issue=8 |pages=1203–12 |date=August 1990 |pmid=2381527 |doi= |url=}}</ref> [[cognitive disorder]] is very common in this disease and can be the presenting sign of it.<ref name="pmid17438218">{{cite journal |vauthors=Murray R, Neumann M, Forman MS, Farmer J, Massimo L, Rice A, Miller BL, Johnson JK, Clark CM, Hurtig HI, Gorno-Tempini ML, Lee VM, Trojanowski JQ, Grossman M |title=Cognitive and motor assessment in autopsy-proven corticobasal degeneration |journal=Neurology |volume=68 |issue=16 |pages=1274–83 |date=April 2007 |pmid=17438218 |doi=10.1212/01.wnl.0000259519.78480.c3 |url=}}</ref><ref name="pmid14639661">{{cite journal |vauthors=Graham NL, Bak TH, Hodges JR |title=Corticobasal degeneration as a cognitive disorder |journal=Mov. Disord. |volume=18 |issue=11 |pages=1224–32 |date=November 2003 |pmid=14639661 |doi=10.1002/mds.10536 |url=}}</ref> there are evidences of asymmetric frontoparietal cortical [[atrophy]] in [[autopsy]] in [[Corticobasal degeneration|CBD]] patients. In microscopic evaluation there are neuronal loss, ballooned achromatic and [[gliosis]].<ref name="pmid9109885">{{cite journal |vauthors=Schneider JA, Watts RL, Gearing M, Brewer RP, Mirra SS |title=Corticobasal degeneration: neuropathologic and clinical heterogeneity |journal=Neurology |volume=48 |issue=4 |pages=959–69 |date=April 1997 |pmid=9109885 |doi= |url=}}</ref><ref name="pmid10489043">{{cite journal |vauthors=Boeve BF, Maraganore DM, Parisi JE, Ahlskog JE, Graff-Radford N, Caselli RJ, Dickson DW, Kokmen E, Petersen RC |title=Pathologic heterogeneity in clinically diagnosed corticobasal degeneration |journal=Neurology |volume=53 |issue=4 |pages=795–800 |date=September 1999 |pmid=10489043 |doi= |url=}}</ref>
===Progressive supranuclear palsy===
*Abnormal [[gait]] is the most common presentation of [[Progressive supranuclear palsy|PSP]] disease. As opposed to idiopathic Parkinson disease, their [[trunk]] is [[Extension|extended]] and [[Arm|arms]] are [[Abduction|abducted]]. They commonly fall from behind leading to [[Bruise|bruises]] and [[lacerations]].<ref name="pmid22166432">{{cite journal |vauthors=Boeve BF |title=Progressive supranuclear palsy |journal=Parkinsonism Relat. Disord. |volume=18 Suppl 1 |issue= |pages=S192–4 |date=January 2012 |pmid=22166432 |doi=10.1016/S1353-8020(11)70060-8 |url=}}</ref> They can also have supranuclear ophthalmoparesis or ophtalmoplegia.<ref name="pmid8648326">{{cite journal |vauthors=Litvan I, Mangone CA, McKee A, Verny M, Parsa A, Jellinger K, D'Olhaberriague L, Chaudhuri KR, Pearce RK |title=Natural history of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) and clinical predictors of survival: a clinicopathological study |journal=J. Neurol. Neurosurg. Psychiatry |volume=60 |issue=6 |pages=615–20 |date=June 1996 |pmid=8648326 |pmc=1073943 |doi= |url=}}</ref>
===Idiopathic and familial basal ganglia calcification===
*Accumulation of [[calcium]] in some [[brain]] regions and the [[basal ganglia]] is known as [[idiopathic basal ganglia calcification]] or bilateral striatopallidodentate calcinosis. Some of these patients can have [[parkinsonism]] symptoms such as [[dystonia]], [[ataxia]] and [[chorea]] mostly between ages 20_60.<ref name="pmid24065723">{{cite journal |vauthors=Nicolas G, Pottier C, Charbonnier C, Guyant-Maréchal L, Le Ber I, Pariente J, Labauge P, Ayrignac X, Defebvre L, Maltête D, Martinaud O, Lefaucheur R, Guillin O, Wallon D, Chaumette B, Rondepierre P, Derache N, Fromager G, Schaeffer S, Krystkowiak P, Verny C, Jurici S, Sauvée M, Vérin M, Lebouvier T, Rouaud O, Thauvin-Robinet C, Rousseau S, Rovelet-Lecrux A, Frebourg T, Campion D, Hannequin D |title=Phenotypic spectrum of probable and genetically-confirmed idiopathic basal ganglia calcification |journal=Brain |volume=136 |issue=Pt 11 |pages=3395–407 |date=November 2013 |pmid=24065723 |doi=10.1093/brain/awt255 |url=}}</ref><ref name="pmid2927646">{{cite journal |vauthors=Ellie E, Julien J, Ferrer X |title=Familial idiopathic striopallidodentate calcifications |journal=Neurology |volume=39 |issue=3 |pages=381–5 |date=March 1989 |pmid=2927646 |doi= |url=}}</ref>
*The [[autosomal dominant]] form of the disease which is known as familial form can be the result of several [[mutations]] such as:<ref name="pmid25686319">{{cite journal |vauthors=Tadic V, Westenberger A, Domingo A, Alvarez-Fischer D, Klein C, Kasten M |title=Primary familial brain calcification with known gene mutations: a systematic review and challenges of phenotypic characterization |journal=JAMA Neurol |volume=72 |issue=4 |pages=460–7 |date=April 2015 |pmid=25686319 |doi=10.1001/jamaneurol.2014.3889 |url=}}</ref>
**The [[SLC20A2]] gene on [[chromosome]] 8p11.2 <ref name="pmid22327515">{{cite journal |vauthors=Wang C, Li Y, Shi L, Ren J, Patti M, Wang T, de Oliveira JR, Sobrido MJ, Quintáns B, Baquero M, Cui X, Zhang XY, Wang L, Xu H, Wang J, Yao J, Dai X, Liu J, Zhang L, Ma H, Gao Y, Ma X, Feng S, Liu M, Wang QK, Forster IC, Zhang X, Liu JY |title=Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis |journal=Nat. Genet. |volume=44 |issue=3 |pages=254–6 |date=February 2012 |pmid=22327515 |doi=10.1038/ng.1077 |url=}}</ref>
**The [[PDGFRB]] gene on [[chromosome]] 5q32 <ref name="pmid23255827">{{cite journal |vauthors=Nicolas G, Pottier C, Maltête D, Coutant S, Rovelet-Lecrux A, Legallic S, Rousseau S, Vaschalde Y, Guyant-Maréchal L, Augustin J, Martinaud O, Defebvre L, Krystkowiak P, Pariente J, Clanet M, Labauge P, Ayrignac X, Lefaucheur R, Le Ber I, Frébourg T, Hannequin D, Campion D |title=Mutation of the PDGFRB gene as a cause of idiopathic basal ganglia calcification |journal=Neurology |volume=80 |issue=2 |pages=181–7 |date=January 2013 |pmid=23255827 |doi=10.1212/WNL.0b013e31827ccf34 |url=}}</ref>
**The [[PDGFB]] gene on [[chromosome]] 22q13.1 <ref name="pmid23913003">{{cite journal |vauthors=Keller A, Westenberger A, Sobrido MJ, García-Murias M, Domingo A, Sears RL, Lemos RR, Ordoñez-Ugalde A, Nicolas G, da Cunha JE, Rushing EJ, Hugelshofer M, Wurnig MC, Kaech A, Reimann R, Lohmann K, Dobričić V, Carracedo A, Petrović I, Miyasaki JM, Abakumova I, Mäe MA, Raschperger E, Zatz M, Zschiedrich K, Klepper J, Spiteri E, Prieto JM, Navas I, Preuss M, Dering C, Janković M, Paucar M, Svenningsson P, Saliminejad K, Khorshid HR, Novaković I, Aguzzi A, Boss A, Le Ber I, Defer G, Hannequin D, Kostić VS, Campion D, Geschwind DH, Coppola G, Betsholtz C, Klein C, Oliveira JR |title=Mutations in the gene encoding PDGF-B cause brain calcifications in humans and mice |journal=Nat. Genet. |volume=45 |issue=9 |pages=1077–82 |date=September 2013 |pmid=23913003 |doi=10.1038/ng.2723 |url=}}</ref><ref name="pmid25832657">{{cite journal |vauthors=Keogh MJ, Pyle A, Daud D, Griffin H, Douroudis K, Eglon G, Miller J, Horvath R, Chinnery PF |title=Clinical heterogeneity of primary familial brain calcification due to a novel mutation in PDGFB |journal=Neurology |volume=84 |issue=17 |pages=1818–20 |date=April 2015 |pmid=25832657 |pmc=4424129 |doi=10.1212/WNL.0000000000001517 |url=}}</ref>
**The XPR1 gene on [[chromosome]] 1q25.3 <ref name="pmid25938945">{{cite journal |vauthors=Legati A, Giovannini D, Nicolas G, López-Sánchez U, Quintáns B, Oliveira JR, Sears RL, Ramos EM, Spiteri E, Sobrido MJ, Carracedo Á, Castro-Fernández C, Cubizolle S, Fogel BL, Goizet C, Jen JC, Kirdlarp S, Lang AE, Miedzybrodzka Z, Mitarnun W, Paucar M, Paulson H, Pariente J, Richard AC, Salins NS, Simpson SA, Striano P, Svenningsson P, Tison F, Unni VK, Vanakker O, Wessels MW, Wetchaphanphesat S, Yang M, Boller F, Campion D, Hannequin D, Sitbon M, Geschwind DH, Battini JL, Coppola G |title=Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export |journal=Nat. Genet. |volume=47 |issue=6 |pages=579–81 |date=June 2015 |pmid=25938945 |pmc=4516721 |doi=10.1038/ng.3289 |url=}}</ref>


==== Essential tremor ====
===Secondary parkinsonism===
[[Essential tremor]] is demonstrated by bilateral resting tremor of arms, [[head]], [[chin]] and [[trunk]]. [[Tremor]] of [[Parkinson's disease|PD]] is action tremor and it seems to be easy to differentiate it from resting tremor of [[Essential tremor|ET]] but sometimes we can see resting tremor in [[Parkinson's disease|PD]] patient and conversely action tremor in [[Essential tremor|ET]] patients.<ref name="pmid10519872">{{cite journal |vauthors=Jankovic J, Schwartz KS, Ondo W |title=Re-emergent tremor of Parkinson's disease |journal=J. Neurol. Neurosurg. Psychiatry |volume=67 |issue=5 |pages=646–50 |date=November 1999 |pmid=10519872 |pmc=1736624 |doi= |url=}}</ref><ref name="pmid11594921">{{cite journal |vauthors=Louis ED, Levy G, Côte LJ, Mejia H, Fahn S, Marder K |title=Clinical correlates of action tremor in Parkinson disease |journal=Arch. Neurol. |volume=58 |issue=10 |pages=1630–4 |date=October 2001 |pmid=11594921 |doi= |url=}}</ref>
*Vascular parkinsonism:<ref name="pmid21885844">{{cite journal |vauthors=Buchman AS, Leurgans SE, Nag S, Bennett DA, Schneider JA |title=Cerebrovascular disease pathology and parkinsonian signs in old age |journal=Stroke |volume=42 |issue=11 |pages=3183–9 |date=November 2011 |pmid=21885844 |pmc=3202031 |doi=10.1161/STROKEAHA.111.623462 |url=}}</ref>
**Some studies suggest that in old ages, microscopic and [[lacunar infarction]] or [[atherosclerosis]] in [[basal ganglia]] can cause [[Parkinsonism]] symptoms.


==== Scans without evidence of dopaminergic deficit (SWEDD) ====
*Drug-induced parkinsonism: <ref name="pmid16361025">{{cite journal |vauthors=Tolosa E, Wenning G, Poewe W |title=The diagnosis of Parkinson's disease |journal=Lancet Neurol |volume=5 |issue=1 |pages=75–86 |date=January 2006 |pmid=16361025 |doi=10.1016/S1474-4422(05)70285-4 |url=}}</ref><ref name="pmid17044803">{{cite journal |vauthors=Mena MA, de Yébenes JG |title=Drug-induced parkinsonism |journal=Expert Opin Drug Saf |volume=5 |issue=6 |pages=759–71 |date=November 2006 |pmid=17044803 |doi=10.1517/14740338.5.6.759 |url=}}</ref><ref name="pmid27779780">{{cite journal |vauthors=Savica R, Grossardt BR, Bower JH, Ahlskog JE, Mielke MM, Rocca WA |title=Incidence and time trends of drug-induced parkinsonism: A 30-year population-based study |journal=Mov. Disord. |volume=32 |issue=2 |pages=227–234 |date=February 2017 |pmid=27779780 |pmc=5318251 |doi=10.1002/mds.26839 |url=}}</ref><ref name="pmid2900293">{{cite journal |vauthors=Hardie RJ, Lees AJ |title=Neuroleptic-induced Parkinson's syndrome: clinical features and results of treatment with levodopa |journal=J. Neurol. Neurosurg. Psychiatry |volume=51 |issue=6 |pages=850–4 |date=June 1988 |pmid=2900293 |pmc=1033159 |doi= |url=}}</ref><ref name="pmid2892586">{{cite journal |vauthors=Jankovic J, Casabona J |title=Coexistent tardive dyskinesia and parkinsonism |journal=Clin Neuropharmacol |volume=10 |issue=6 |pages=511–21 |date=December 1987 |pmid=2892586 |doi= |url=}}</ref>
Patients with scans without evidence of dopaminergic deficit have [[upper extremity]] resting [[tremor]] but their disease does not progress to the complete [[Parkinson's disease|PD]] and there are no evidence of [[dopamine]] depletion in their [[Nigrostriatal pathway|NS]].<ref name="pmid17712858">{{cite journal |vauthors=Schneider SA, Edwards MJ, Mir P, Cordivari C, Hooker J, Dickson J, Quinn N, Bhatia KP |title=Patients with adult-onset dystonic tremor resembling parkinsonian tremor have scans without evidence of dopaminergic deficit (SWEDDs) |journal=Mov. Disord. |volume=22 |issue=15 |pages=2210–5 |date=November 2007 |pmid=17712858 |doi=10.1002/mds.21685 |url=}}</ref>
**The most common type of [[secondary parkinsonism]] is drug induced PD.
 
***[[Antiemetic]] and [[Antipsychotics|antipsychotic]] drugs are mostly the cause.
==== Dementia with Lewy bodies ====
**They can cause [[akathisia]] and [[orofacial dyskinesia]] which in these cases we can differentiate them from idiopathic [[Parkinson's disease|PD]] but sometimes they are similar to [[Parkinson's disease|PD]] and have symmetrical resting [[tremor]].
[[Dementia]] will finally occurs in the most cases of [[Parkinson's disease|Parkinson disease]] but the timing of [[dementia]] in [[Parkinson's disease|PD]] is after full developing of [[Parkinson's disease|PD]] and mostly after at least one year of disease start date. When [[dementia]] occurs with or before the [[signs]] and [[symptoms]] of [[Parkinson's disease|Parkinson disease]] we will categorize it as [[Dementia With Lewy Bodies|dementia with lewy body]].<ref name="pmid28592453">{{cite journal |vauthors=McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems J, Ballard CG, Bayston A, Beach TG, Blanc F, Bohnen N, Bonanni L, Bras J, Brundin P, Burn D, Chen-Plotkin A, Duda JE, El-Agnaf O, Feldman H, Ferman TJ, Ffytche D, Fujishiro H, Galasko D, Goldman JG, Gomperts SN, Graff-Radford NR, Honig LS, Iranzo A, Kantarci K, Kaufer D, Kukull W, Lee VMY, Leverenz JB, Lewis S, Lippa C, Lunde A, Masellis M, Masliah E, McLean P, Mollenhauer B, Montine TJ, Moreno E, Mori E, Murray M, O'Brien JT, Orimo S, Postuma RB, Ramaswamy S, Ross OA, Salmon DP, Singleton A, Taylor A, Thomas A, Tiraboschi P, Toledo JB, Trojanowski JQ, Tsuang D, Walker Z, Yamada M, Kosaka K |title=Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium |journal=Neurology |volume=89 |issue=1 |pages=88–100 |date=July 2017 |pmid=28592453 |pmc=5496518 |doi=10.1212/WNL.0000000000004058 |url=}}</ref><ref name="pmid27492190">{{cite journal |vauthors=Boeve BF, Dickson DW, Duda JE, Ferman TJ, Galasko DR, Galvin JE, Goldman JG, Growdon JH, Hurtig HI, Kaufer DI, Kantarci K, Leverenz JB, Lippa CF, Lopez OL, McKeith IG, Singleton AB, Taylor A, Tsuang D, Weintraub D, Zabetian CP |title=Arguing against the proposed definition changes of PD |journal=Mov. Disord. |volume=31 |issue=11 |pages=1619–1622 |date=November 2016 |pmid=27492190 |pmc=5168716 |doi=10.1002/mds.26721 |url=}}</ref>
 
==== Multiple system atrophy ====
[[Multiple system atrophy|MSA]] is an [[idiopathic]] disease<ref name="pmid18825660">{{cite journal |vauthors=Wenning GK, Stefanova N, Jellinger KA, Poewe W, Schlossmacher MG |title=Multiple system atrophy: a primary oligodendrogliopathy |journal=Ann. Neurol. |volume=64 |issue=3 |pages=239–46 |date=September 2008 |pmid=18825660 |doi=10.1002/ana.21465 |url=}}</ref> characterized by [[Autonomic nervous system|autonomic]] problems such as [[urogenital]] dysfunction, [[ataxia]] and [[parkinsonism]] [[symptoms]].<ref name="pmid19909915">{{cite journal |vauthors=Stefanova N, Bücke P, Duerr S, Wenning GK |title=Multiple system atrophy: an update |journal=Lancet Neurol |volume=8 |issue=12 |pages=1172–8 |date=December 2009 |pmid=19909915 |doi=10.1016/S1474-4422(09)70288-1 |url=}}</ref> [[Multiple system atrophy|MSA]] patients have resting [[tremor]] in arms, rigidity and [[bradykinesia]].<ref name="pmid16049636">{{cite journal |vauthors=Geser F, Seppi K, Stampfer-Kountchev M, Köllensperger M, Diem A, Ndayisaba JP, Ostergaard K, Dupont E, Cardozo A, Tolosa E, Abele M, Dodel R, Klockgether T, Ghorayeb I, Yekhlef F, Tison F, Daniels C, Kopper F, Deuschl G, Coelho M, Ferreira J, Rosa MM, Sampaio C, Bozi M, Schrag A, Hooker J, Kim H, Scaravilli T, Mathias CJ, Fowler C, Wood N, Quinn N, Widner H, Nilsson CF, Lindvall O, Schimke N, Eggert KM, Oertel W, del Sorbo F, Carella F, Albanese A, Pellecchia MT, Barone P, Djaldetti R, Meco G, Colosimo C, Gonzalez-Mandly A, Berciano J, Gurevich T, Giladi N, Galitzky M, Ory F, Rascol O, Kamm C, Buerk K, Maass S, Gasser T, Poewe W, Wenning GK |title=The European Multiple System Atrophy-Study Group (EMSA-SG) |journal=J Neural Transm (Vienna) |volume=112 |issue=12 |pages=1677–86 |date=December 2005 |pmid=16049636 |doi=10.1007/s00702-005-0328-y |url=}}</ref> The underlying [[pathophysiology]] of [[Multiple system atrophy|MSA]] is [[myelin]] dysfunction and [[inclusions]] in [[glial cell]] throughout [[CNS]].<ref name="pmid18825660">{{cite journal |vauthors=Wenning GK, Stefanova N, Jellinger KA, Poewe W, Schlossmacher MG |title=Multiple system atrophy: a primary oligodendrogliopathy |journal=Ann. Neurol. |volume=64 |issue=3 |pages=239–46 |date=September 2008 |pmid=18825660 |doi=10.1002/ana.21465 |url=}}</ref><ref name="pmid9736024">{{cite journal |vauthors=Matsuo A, Akiguchi I, Lee GC, McGeer EG, McGeer PL, Kimura J |title=Myelin degeneration in multiple system atrophy detected by unique antibodies |journal=Am. J. Pathol. |volume=153 |issue=3 |pages=735–44 |date=September 1998 |pmid=9736024 |pmc=1853025 |doi=10.1016/S0002-9440(10)65617-9 |url=}}</ref>
 
==== Corticobasal degeneration ====
 
==== Progressive supranuclear palsy ====
 
==== Idiopathic and familial basal ganglia calcification ====
Accumulation of [[calcium]] in some [[brain]] regions and the [[basal ganglia]] is known as [[idiopathic basal ganglia calcification]] or bilateral striatopallidodentate calcinosis. Some of these patients can have [[parkinsonism]] symptoms such as [[dystonia]], [[ataxia]] and [[chorea]] mostly between ages 20_60.<ref name="pmid24065723">{{cite journal |vauthors=Nicolas G, Pottier C, Charbonnier C, Guyant-Maréchal L, Le Ber I, Pariente J, Labauge P, Ayrignac X, Defebvre L, Maltête D, Martinaud O, Lefaucheur R, Guillin O, Wallon D, Chaumette B, Rondepierre P, Derache N, Fromager G, Schaeffer S, Krystkowiak P, Verny C, Jurici S, Sauvée M, Vérin M, Lebouvier T, Rouaud O, Thauvin-Robinet C, Rousseau S, Rovelet-Lecrux A, Frebourg T, Campion D, Hannequin D |title=Phenotypic spectrum of probable and genetically-confirmed idiopathic basal ganglia calcification |journal=Brain |volume=136 |issue=Pt 11 |pages=3395–407 |date=November 2013 |pmid=24065723 |doi=10.1093/brain/awt255 |url=}}</ref><ref name="pmid2927646">{{cite journal |vauthors=Ellie E, Julien J, Ferrer X |title=Familial idiopathic striopallidodentate calcifications |journal=Neurology |volume=39 |issue=3 |pages=381–5 |date=March 1989 |pmid=2927646 |doi= |url=}}</ref> The [[autosomal dominant]] form of the disease which is known as familial form<ref name="pmid25686319">{{cite journal |vauthors=Tadic V, Westenberger A, Domingo A, Alvarez-Fischer D, Klein C, Kasten M |title=Primary familial brain calcification with known gene mutations: a systematic review and challenges of phenotypic characterization |journal=JAMA Neurol |volume=72 |issue=4 |pages=460–7 |date=April 2015 |pmid=25686319 |doi=10.1001/jamaneurol.2014.3889 |url=}}</ref> can be the result of several [[mutations]] such as: The [[SLC20A2]] gene on [[chromosome]] 8p11.2<ref name="pmid22327515">{{cite journal |vauthors=Wang C, Li Y, Shi L, Ren J, Patti M, Wang T, de Oliveira JR, Sobrido MJ, Quintáns B, Baquero M, Cui X, Zhang XY, Wang L, Xu H, Wang J, Yao J, Dai X, Liu J, Zhang L, Ma H, Gao Y, Ma X, Feng S, Liu M, Wang QK, Forster IC, Zhang X, Liu JY |title=Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis |journal=Nat. Genet. |volume=44 |issue=3 |pages=254–6 |date=February 2012 |pmid=22327515 |doi=10.1038/ng.1077 |url=}}</ref>, the [[PDGFRB]] gene on [[chromosome]] 5q32<ref name="pmid23255827">{{cite journal |vauthors=Nicolas G, Pottier C, Maltête D, Coutant S, Rovelet-Lecrux A, Legallic S, Rousseau S, Vaschalde Y, Guyant-Maréchal L, Augustin J, Martinaud O, Defebvre L, Krystkowiak P, Pariente J, Clanet M, Labauge P, Ayrignac X, Lefaucheur R, Le Ber I, Frébourg T, Hannequin D, Campion D |title=Mutation of the PDGFRB gene as a cause of idiopathic basal ganglia calcification |journal=Neurology |volume=80 |issue=2 |pages=181–7 |date=January 2013 |pmid=23255827 |doi=10.1212/WNL.0b013e31827ccf34 |url=}}</ref>, the [[PDGFB]] gene on [[chromosome]] 22q13.1<ref name="pmid23913003">{{cite journal |vauthors=Keller A, Westenberger A, Sobrido MJ, García-Murias M, Domingo A, Sears RL, Lemos RR, Ordoñez-Ugalde A, Nicolas G, da Cunha JE, Rushing EJ, Hugelshofer M, Wurnig MC, Kaech A, Reimann R, Lohmann K, Dobričić V, Carracedo A, Petrović I, Miyasaki JM, Abakumova I, Mäe MA, Raschperger E, Zatz M, Zschiedrich K, Klepper J, Spiteri E, Prieto JM, Navas I, Preuss M, Dering C, Janković M, Paucar M, Svenningsson P, Saliminejad K, Khorshid HR, Novaković I, Aguzzi A, Boss A, Le Ber I, Defer G, Hannequin D, Kostić VS, Campion D, Geschwind DH, Coppola G, Betsholtz C, Klein C, Oliveira JR |title=Mutations in the gene encoding PDGF-B cause brain calcifications in humans and mice |journal=Nat. Genet. |volume=45 |issue=9 |pages=1077–82 |date=September 2013 |pmid=23913003 |doi=10.1038/ng.2723 |url=}}</ref><ref name="pmid25832657">{{cite journal |vauthors=Keogh MJ, Pyle A, Daud D, Griffin H, Douroudis K, Eglon G, Miller J, Horvath R, Chinnery PF |title=Clinical heterogeneity of primary familial brain calcification due to a novel mutation in PDGFB |journal=Neurology |volume=84 |issue=17 |pages=1818–20 |date=April 2015 |pmid=25832657 |pmc=4424129 |doi=10.1212/WNL.0000000000001517 |url=}}</ref> and the XPR1 gene on [[chromosome]] 1q25.3.<ref name="pmid25938945">{{cite journal |vauthors=Legati A, Giovannini D, Nicolas G, López-Sánchez U, Quintáns B, Oliveira JR, Sears RL, Ramos EM, Spiteri E, Sobrido MJ, Carracedo Á, Castro-Fernández C, Cubizolle S, Fogel BL, Goizet C, Jen JC, Kirdlarp S, Lang AE, Miedzybrodzka Z, Mitarnun W, Paucar M, Paulson H, Pariente J, Richard AC, Salins NS, Simpson SA, Striano P, Svenningsson P, Tison F, Unni VK, Vanakker O, Wessels MW, Wetchaphanphesat S, Yang M, Boller F, Campion D, Hannequin D, Sitbon M, Geschwind DH, Battini JL, Coppola G |title=Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export |journal=Nat. Genet. |volume=47 |issue=6 |pages=579–81 |date=June 2015 |pmid=25938945 |pmc=4516721 |doi=10.1038/ng.3289 |url=}}</ref>
 
==== Other neurodegenerative disorders ====
 
==== Secondary parkinsonism ====
* Vascular parkinsonism: Some studies suggest that in old ages, microscopic and [[lacunar infarction]] or [[atherosclerosis]] in [[basal ganglia]] can cause [[Parkinsonism]] symptoms.<ref name="pmid21885844">{{cite journal |vauthors=Buchman AS, Leurgans SE, Nag S, Bennett DA, Schneider JA |title=Cerebrovascular disease pathology and parkinsonian signs in old age |journal=Stroke |volume=42 |issue=11 |pages=3183–9 |date=November 2011 |pmid=21885844 |pmc=3202031 |doi=10.1161/STROKEAHA.111.623462 |url=}}</ref>
* Drug-induced parkinsonism


==References==
==References==

Latest revision as of 14:39, 6 August 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

Parkinson disease must be differentiated from other diseases that can mimic this disease clinically or radiologically such as: essential tremor, scans without evidence of dopaminergic deficit (SWEDD), dementia with Lewy bodies, multiple system atrophy, corticobasal degeneration, progressive supranuclear palsy, idiopathic and familial basal ganglia calcification, and secondary parkinsonism.

Differential Diagnosis

  • Parkinson disease must be differentiated from other diseases that can mimic this disease clinically or radiologically such as:

Essential tremor

  • Essential tremor is demonstrated by bilateral resting tremor of arms, head, chin and trunk. Tremor of PD is action tremor and it seems to be easy to differentiate it from resting tremor of ET but sometimes we can see resting tremor in PD patient and conversely action tremor in ET patients.[1][2]

Scans without evidence of dopaminergic deficit (SWEDD)

  • Patients with scans without evidence of dopaminergic deficit have upper extremity resting tremor but their disease does not progress to the complete PD and there are no evidence of dopamine depletion in their NS.[3]

Dementia with Lewy bodies

Multiple system atrophy

Corticobasal degeneration

Progressive supranuclear palsy

  • Abnormal gait is the most common presentation of PSP disease. As opposed to idiopathic Parkinson disease, their trunk is extended and arms are abducted. They commonly fall from behind leading to bruises and lacerations.[17] They can also have supranuclear ophthalmoparesis or ophtalmoplegia.[18]

Idiopathic and familial basal ganglia calcification

Secondary parkinsonism

References

  1. ↑ Jankovic J, Schwartz KS, Ondo W (November 1999). "Re-emergent tremor of Parkinson's disease". J. Neurol. Neurosurg. Psychiatry. 67 (5): 646–50. PMC 1736624. PMID 10519872.
  2. ↑ Louis ED, Levy G, Côte LJ, Mejia H, Fahn S, Marder K (October 2001). "Clinical correlates of action tremor in Parkinson disease". Arch. Neurol. 58 (10): 1630–4. PMID 11594921.
  3. ↑ Schneider SA, Edwards MJ, Mir P, Cordivari C, Hooker J, Dickson J, Quinn N, Bhatia KP (November 2007). "Patients with adult-onset dystonic tremor resembling parkinsonian tremor have scans without evidence of dopaminergic deficit (SWEDDs)". Mov. Disord. 22 (15): 2210–5. doi:10.1002/mds.21685. PMID 17712858.
  4. ↑ McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, Aarsland D, Galvin J, Attems J, Ballard CG, Bayston A, Beach TG, Blanc F, Bohnen N, Bonanni L, Bras J, Brundin P, Burn D, Chen-Plotkin A, Duda JE, El-Agnaf O, Feldman H, Ferman TJ, Ffytche D, Fujishiro H, Galasko D, Goldman JG, Gomperts SN, Graff-Radford NR, Honig LS, Iranzo A, Kantarci K, Kaufer D, Kukull W, Lee V, Leverenz JB, Lewis S, Lippa C, Lunde A, Masellis M, Masliah E, McLean P, Mollenhauer B, Montine TJ, Moreno E, Mori E, Murray M, O'Brien JT, Orimo S, Postuma RB, Ramaswamy S, Ross OA, Salmon DP, Singleton A, Taylor A, Thomas A, Tiraboschi P, Toledo JB, Trojanowski JQ, Tsuang D, Walker Z, Yamada M, Kosaka K (July 2017). "Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium". Neurology. 89 (1): 88–100. doi:10.1212/WNL.0000000000004058. PMC 5496518. PMID 28592453. Vancouver style error: initials (help)
  5. ↑ Boeve BF, Dickson DW, Duda JE, Ferman TJ, Galasko DR, Galvin JE, Goldman JG, Growdon JH, Hurtig HI, Kaufer DI, Kantarci K, Leverenz JB, Lippa CF, Lopez OL, McKeith IG, Singleton AB, Taylor A, Tsuang D, Weintraub D, Zabetian CP (November 2016). "Arguing against the proposed definition changes of PD". Mov. Disord. 31 (11): 1619–1622. doi:10.1002/mds.26721. PMC 5168716. PMID 27492190.
  6. ↑ 6.0 6.1 Wenning GK, Stefanova N, Jellinger KA, Poewe W, Schlossmacher MG (September 2008). "Multiple system atrophy: a primary oligodendrogliopathy". Ann. Neurol. 64 (3): 239–46. doi:10.1002/ana.21465. PMID 18825660.
  7. ↑ Stefanova N, Bücke P, Duerr S, Wenning GK (December 2009). "Multiple system atrophy: an update". Lancet Neurol. 8 (12): 1172–8. doi:10.1016/S1474-4422(09)70288-1. PMID 19909915.
  8. ↑ Geser F, Seppi K, Stampfer-Kountchev M, Köllensperger M, Diem A, Ndayisaba JP, Ostergaard K, Dupont E, Cardozo A, Tolosa E, Abele M, Dodel R, Klockgether T, Ghorayeb I, Yekhlef F, Tison F, Daniels C, Kopper F, Deuschl G, Coelho M, Ferreira J, Rosa MM, Sampaio C, Bozi M, Schrag A, Hooker J, Kim H, Scaravilli T, Mathias CJ, Fowler C, Wood N, Quinn N, Widner H, Nilsson CF, Lindvall O, Schimke N, Eggert KM, Oertel W, del Sorbo F, Carella F, Albanese A, Pellecchia MT, Barone P, Djaldetti R, Meco G, Colosimo C, Gonzalez-Mandly A, Berciano J, Gurevich T, Giladi N, Galitzky M, Ory F, Rascol O, Kamm C, Buerk K, Maass S, Gasser T, Poewe W, Wenning GK (December 2005). "The European Multiple System Atrophy-Study Group (EMSA-SG)". J Neural Transm (Vienna). 112 (12): 1677–86. doi:10.1007/s00702-005-0328-y. PMID 16049636.
  9. ↑ Matsuo A, Akiguchi I, Lee GC, McGeer EG, McGeer PL, Kimura J (September 1998). "Myelin degeneration in multiple system atrophy detected by unique antibodies". Am. J. Pathol. 153 (3): 735–44. doi:10.1016/S0002-9440(10)65617-9. PMC 1853025. PMID 9736024.
  10. ↑ Rebeiz JJ, Kolodny EH, Richardson EP (January 1968). "Corticodentatonigral degeneration with neuronal achromasia". Arch. Neurol. 18 (1): 20–33. PMID 5634369.
  11. ↑ Wenning GK, Litvan I, Jankovic J, Granata R, Mangone CA, McKee A, Poewe W, Jellinger K, Ray Chaudhuri K, D'Olhaberriague L, Pearce RK (February 1998). "Natural history and survival of 14 patients with corticobasal degeneration confirmed at postmortem examination". J. Neurol. Neurosurg. Psychiatry. 64 (2): 184–9. PMC 2169933. PMID 9489528.
  12. ↑ Riley DE, Lang AE, Lewis A, Resch L, Ashby P, Hornykiewicz O, Black S (August 1990). "Cortical-basal ganglionic degeneration". Neurology. 40 (8): 1203–12. PMID 2381527.
  13. ↑ Murray R, Neumann M, Forman MS, Farmer J, Massimo L, Rice A, Miller BL, Johnson JK, Clark CM, Hurtig HI, Gorno-Tempini ML, Lee VM, Trojanowski JQ, Grossman M (April 2007). "Cognitive and motor assessment in autopsy-proven corticobasal degeneration". Neurology. 68 (16): 1274–83. doi:10.1212/01.wnl.0000259519.78480.c3. PMID 17438218.
  14. ↑ Graham NL, Bak TH, Hodges JR (November 2003). "Corticobasal degeneration as a cognitive disorder". Mov. Disord. 18 (11): 1224–32. doi:10.1002/mds.10536. PMID 14639661.
  15. ↑ Schneider JA, Watts RL, Gearing M, Brewer RP, Mirra SS (April 1997). "Corticobasal degeneration: neuropathologic and clinical heterogeneity". Neurology. 48 (4): 959–69. PMID 9109885.
  16. ↑ Boeve BF, Maraganore DM, Parisi JE, Ahlskog JE, Graff-Radford N, Caselli RJ, Dickson DW, Kokmen E, Petersen RC (September 1999). "Pathologic heterogeneity in clinically diagnosed corticobasal degeneration". Neurology. 53 (4): 795–800. PMID 10489043.
  17. ↑ Boeve BF (January 2012). "Progressive supranuclear palsy". Parkinsonism Relat. Disord. 18 Suppl 1: S192–4. doi:10.1016/S1353-8020(11)70060-8. PMID 22166432.
  18. ↑ Litvan I, Mangone CA, McKee A, Verny M, Parsa A, Jellinger K, D'Olhaberriague L, Chaudhuri KR, Pearce RK (June 1996). "Natural history of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) and clinical predictors of survival: a clinicopathological study". J. Neurol. Neurosurg. Psychiatry. 60 (6): 615–20. PMC 1073943. PMID 8648326.
  19. ↑ Nicolas G, Pottier C, Charbonnier C, Guyant-Maréchal L, Le Ber I, Pariente J, Labauge P, Ayrignac X, Defebvre L, Maltête D, Martinaud O, Lefaucheur R, Guillin O, Wallon D, Chaumette B, Rondepierre P, Derache N, Fromager G, Schaeffer S, Krystkowiak P, Verny C, Jurici S, Sauvée M, Vérin M, Lebouvier T, Rouaud O, Thauvin-Robinet C, Rousseau S, Rovelet-Lecrux A, Frebourg T, Campion D, Hannequin D (November 2013). "Phenotypic spectrum of probable and genetically-confirmed idiopathic basal ganglia calcification". Brain. 136 (Pt 11): 3395–407. doi:10.1093/brain/awt255. PMID 24065723.
  20. ↑ Ellie E, Julien J, Ferrer X (March 1989). "Familial idiopathic striopallidodentate calcifications". Neurology. 39 (3): 381–5. PMID 2927646.
  21. ↑ Tadic V, Westenberger A, Domingo A, Alvarez-Fischer D, Klein C, Kasten M (April 2015). "Primary familial brain calcification with known gene mutations: a systematic review and challenges of phenotypic characterization". JAMA Neurol. 72 (4): 460–7. doi:10.1001/jamaneurol.2014.3889. PMID 25686319.
  22. ↑ Wang C, Li Y, Shi L, Ren J, Patti M, Wang T, de Oliveira JR, Sobrido MJ, Quintáns B, Baquero M, Cui X, Zhang XY, Wang L, Xu H, Wang J, Yao J, Dai X, Liu J, Zhang L, Ma H, Gao Y, Ma X, Feng S, Liu M, Wang QK, Forster IC, Zhang X, Liu JY (February 2012). "Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis". Nat. Genet. 44 (3): 254–6. doi:10.1038/ng.1077. PMID 22327515.
  23. ↑ Nicolas G, Pottier C, Maltête D, Coutant S, Rovelet-Lecrux A, Legallic S, Rousseau S, Vaschalde Y, Guyant-Maréchal L, Augustin J, Martinaud O, Defebvre L, Krystkowiak P, Pariente J, Clanet M, Labauge P, Ayrignac X, Lefaucheur R, Le Ber I, Frébourg T, Hannequin D, Campion D (January 2013). "Mutation of the PDGFRB gene as a cause of idiopathic basal ganglia calcification". Neurology. 80 (2): 181–7. doi:10.1212/WNL.0b013e31827ccf34. PMID 23255827.
  24. ↑ Keller A, Westenberger A, Sobrido MJ, García-Murias M, Domingo A, Sears RL, Lemos RR, Ordoñez-Ugalde A, Nicolas G, da Cunha JE, Rushing EJ, Hugelshofer M, Wurnig MC, Kaech A, Reimann R, Lohmann K, Dobričić V, Carracedo A, Petrović I, Miyasaki JM, Abakumova I, Mäe MA, Raschperger E, Zatz M, Zschiedrich K, Klepper J, Spiteri E, Prieto JM, Navas I, Preuss M, Dering C, Janković M, Paucar M, Svenningsson P, Saliminejad K, Khorshid HR, Novaković I, Aguzzi A, Boss A, Le Ber I, Defer G, Hannequin D, Kostić VS, Campion D, Geschwind DH, Coppola G, Betsholtz C, Klein C, Oliveira JR (September 2013). "Mutations in the gene encoding PDGF-B cause brain calcifications in humans and mice". Nat. Genet. 45 (9): 1077–82. doi:10.1038/ng.2723. PMID 23913003.
  25. ↑ Keogh MJ, Pyle A, Daud D, Griffin H, Douroudis K, Eglon G, Miller J, Horvath R, Chinnery PF (April 2015). "Clinical heterogeneity of primary familial brain calcification due to a novel mutation in PDGFB". Neurology. 84 (17): 1818–20. doi:10.1212/WNL.0000000000001517. PMC 4424129. PMID 25832657.
  26. ↑ Legati A, Giovannini D, Nicolas G, López-Sánchez U, Quintáns B, Oliveira JR, Sears RL, Ramos EM, Spiteri E, Sobrido MJ, Carracedo Á, Castro-Fernández C, Cubizolle S, Fogel BL, Goizet C, Jen JC, Kirdlarp S, Lang AE, Miedzybrodzka Z, Mitarnun W, Paucar M, Paulson H, Pariente J, Richard AC, Salins NS, Simpson SA, Striano P, Svenningsson P, Tison F, Unni VK, Vanakker O, Wessels MW, Wetchaphanphesat S, Yang M, Boller F, Campion D, Hannequin D, Sitbon M, Geschwind DH, Battini JL, Coppola G (June 2015). "Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export". Nat. Genet. 47 (6): 579–81. doi:10.1038/ng.3289. PMC 4516721. PMID 25938945.
  27. ↑ Buchman AS, Leurgans SE, Nag S, Bennett DA, Schneider JA (November 2011). "Cerebrovascular disease pathology and parkinsonian signs in old age". Stroke. 42 (11): 3183–9. doi:10.1161/STROKEAHA.111.623462. PMC 3202031. PMID 21885844.
  28. ↑ Tolosa E, Wenning G, Poewe W (January 2006). "The diagnosis of Parkinson's disease". Lancet Neurol. 5 (1): 75–86. doi:10.1016/S1474-4422(05)70285-4. PMID 16361025.
  29. ↑ Mena MA, de Yébenes JG (November 2006). "Drug-induced parkinsonism". Expert Opin Drug Saf. 5 (6): 759–71. doi:10.1517/14740338.5.6.759. PMID 17044803.
  30. ↑ Savica R, Grossardt BR, Bower JH, Ahlskog JE, Mielke MM, Rocca WA (February 2017). "Incidence and time trends of drug-induced parkinsonism: A 30-year population-based study". Mov. Disord. 32 (2): 227–234. doi:10.1002/mds.26839. PMC 5318251. PMID 27779780.
  31. ↑ Hardie RJ, Lees AJ (June 1988). "Neuroleptic-induced Parkinson's syndrome: clinical features and results of treatment with levodopa". J. Neurol. Neurosurg. Psychiatry. 51 (6): 850–4. PMC 1033159. PMID 2900293.
  32. ↑ Jankovic J, Casabona J (December 1987). "Coexistent tardive dyskinesia and parkinsonism". Clin Neuropharmacol. 10 (6): 511–21. PMID 2892586.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Parkinson%27s_disease_differential_diagnosis&oldid=1578493"