Millest räägime? Miks tekib Parkinsoni tõbi? kiire meeldetuletus taastusravi meeskonnale. Parkinsoni tõve avastamislugu
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1 Millest räägime? Miks tekib Parkinsoni tõbi? kiire meeldetuletus taastusravi meeskonnale. Egle Seppo Taastusarst AS Keila Taastusravikeskus Ajaloost Epidemioloogiast Anatoomiast Etiopatogeneesist Sümptomaatikast Diagnoosimisest Parkinsoni tõve avastamislugu sajand BC papüürus ürikud Egiptusest 10 sajand BC India Ayurveda meditsiin Kampa vata 175. AD kirjeldas Claudius Galenus rahuoleku treemor, kehatüve ebalus, halvatus 1817 James Parkinson Essay on the Shaking Palsy 1872 Jean-Martin Charcot Parkinsoni tõbi Revolutsioon Parkinsoni tõve ajaloos 1897 Edouard Brissaud subthalamuse või pedunculus cerebri isheemiline kahjustus? 1912 Frederic Lewy patoloogilised muutused ajus Lewy kehakesed 1919 Konstantin Tretiakoff substantia nigra publitseeris Rolf Hassler 1950 Arvid Carlsson dopamiini roll haiguse tekkes -> Nobeli preemia 1994 Alice Lazzarini meeskonnaga määratles haiguse geneetilise komponendi 1
2 Mõned faktid ravi ajaloost Kuulsaid parkinsonihaigeid Mucuna viljad Ajurveda meditsiinis 19.sajandil antikolinergilised alkaloidid 1911 sünteesiti Levodopa Casimir Funk i poolt 1967 Levodopa kliinilises praktikas 1939 esimesed kirurgilised katsetused 1980ndate lõpp aju süvastimulatsioon -> FDA poolt kliinilisse katsetusse 1997 Kuulsaid parkinsonihaigeid Parkinsoni tõve epidemioloogia 2. enamlevinud neurodegeneratiivne haigus 1% > 60 aastaste elanikkonnast 7-10 milj. inimest kogu maailmas WHO -> tõsine tervishoiuprobleem vananevas ühiskonnas Europiidne rass enam Levimus / , indoeuroopas / Eestis 152/ ; 16.6/ aastas Neuroanatoomia 2
3 Neuroanatoomia - basaalganglionid Neuroanatoomia 3
4 Neurotransmitterid Neurotransmitter Funktsioon Sekretsiooni koht Atsetüülkoliin Pidurdav/erutav CNS/PNS Biogeensed amiinid Noradrenaliin/Adrenaliin Erutav/pidurdav CNS/PNS Dopamiin Pidurdav/erutav CNS/PNS Serotoniin Pidurdav CNS Aminohapped GABA Pidurdav CNS Gly Pidurdav CNS Glu Erutav CNS Asp Erutav CNS Neuropeptiidid VIP, SubstantsP, enkefaliinid Pidurdav/erutav CNS/PNS C₈H₁₁NO₂ Dopamiin Dopamiin Peaaju närvilõpmed Väljaspool närvisüsteemi Veresoonkond vasodilataator -> vasopressoorne ja inotroopne efekt (positiivne kronotroopne ja inotroopne toime) Hingamiselundkond Neerud - diureesi Kõhunääre väheneb insuliini produktsioon Seedetrakt aeglustab soole motoorikat Immuunsüsteem - Ly ak ivsust Mida dopamiin teeb peaajus? Motoorika kontroll Kognitsioon Motivatsioon Õppimisvõime Uni Käitumine Sarrustusvõime Meeleolu Tähelepanu Dopamiini süntees 4
5 Kuidas tekib liigutus? erutav pidurdav LCS ja RS tract Peamised neurotransmitterid Pidurdavad (GABA, Dopamiin) Erutavad (Glutamaat, Dopamiin) Indirect Putamen Direct Pidurdus: Vähenenud pidurdus = tugevam vastusreaktsioon Suurenenud pidurdus = nõrgem vastusreaktsioon Erutus: Vähenenud erutus = nõrgem vastusreaktsioon Suurenenud erutus = tugevam vastusreaktsioon GP ext Nucl.Subth. SNpars comp Basal ganglia GP int Mot.Thalamus vlppn dppn erutav pidurdav Putamen Indirect SNpars comp GP ext Nucl.Subth. Basal ganglia Direct GP int LCS ja RS tract Mot.Thalamus vlppn dppn Pidurduse tulemusel: Thalamus vlppn Põhjus Ajukoore motoorsete keskuste erutuvuse Retikulospinaaltrakti aktiivsuse muutus, LMN Tulemus Vähenenud tahtelised liigutused: bradükineesia ja akineesia Lihasrigiidsus posturaalsetes ja jäsemelihastes dppn ülekanne RF Kõnnimustri häirumine Parkinsonitõve riskifaktorid Vanus Perekondlik anamnees Sugu Rass Tööstusmürgid(MPTP) ja pestitsiidid (Serotone, benomüül) Eluanamnees (peatrauma, isiksuse omadused?, emotsionaalne stress?) B-vitamiini, foolhappe puudus? Häirunud östrogeenide produktsioon? Parkinsonitõve etioloogilised faktorid Pärilikkus α-synuclein/sncaprotein/park1 4.krom; AD PARKIN/PARK2-6.krom; AR PINK1/PARK6 1.krom; AR LRRK2/PARK8 12.krom; AD DJ-1/PARK7-1.krom; AR Glycocerebrosidas 1.krom; AD UCH-L1/PARK5(ubikvitiin proteolüütilise süsteemi ensüüm) vähenenud ensüümi aktiivsus; 4.krom Omi/HtrA2(apoptoosi inhibiitor) Nurr1(dopaminergilise tasakaalu säilitamine)- 2.krom mtdna polymerasγ/polg1 15.krom "Etiology and Pathogenesis of PD"; Neurol.Clin 27(2009)
6 Henchcliffe C and Beal MF (2008) Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis Nat Clin Pract Neurol /ncpneuro0924 Parkinsonitõve patogenees Parkinsoni tõve sümptomaatika UK Parkinsonitõve Seltsi Ajupanga Diagnoosikriteeriumid (UK PDS BB) Parkinsonistliku sündroomi diagnoos Välistavad kriteeriumid Toetavad kriteeriumid Henchcliffe C and Beal MF (2008) Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis Nat Clin Pract Neurol /ncpneuro0924 Parkinsoni tõve Eesti ravijuhend 2008 EFNS/MDS-ES recommendations for the diagnosis of Parkinson s disease 2012 Parkinsonistliku sündroomi diagnoos: Bradükineesia ja vähemalt üks järgnevatest: Lihasrigiidsus 4-6Hz rahutreemor Posturaalne ebastabiilsus, mis ei ole põhjustatud primaarse nägemis-, vestibulaarse, tserebellaarse ega propriotseptiivse funktsiooni häirest 6
7 Välistavad kriteeriumid: Korduvad insuldid anamneesis parkinsonismi süvenemisega Korduvad peatraumad anamneesis Entsefaliit anamneesis Oculogyric crisis ( ) Neuroleptikumravi sümptomite tekkimise ajal >1 sugulane sama haigusega ( ) Püsiv remissioon Püsiv ühepoolne haaratus 3 aastat peale haiguse algust Supranukleaarne halvatus Tserebellaarsed nähud Varajane autonoomse NS haaratus Varane raske dementsus Babinski refleks Tuumor või hüdrotseefalus CT-uuringul Puudulik vastus L-dopa suurtele annustele (malabsorptsiooni puudumisel) Toksiliste ainete toime (MPTP) ( ) EFNS/MDS-ES Toetavad kriteeriumid: Kindla Parkinsonitõve diagnoosiks nõutav 3 või enama kriteeriumi esinemine: Ühepoolne haiguse algus Esineb rahutreemor Progresseeruv kulg Püsiv sümptomite asümmeetria (väljendunum kehapoolel, kus tekkisid esmassümptomid) ( ) Levodopa hea toimeefekt (70-100%) Rasked levodopast tingitud düskineesiad Levodopa toimeefekt >5 aasta ( ) Haiguse kliiniline kulg >10 aasta ( ) Hüposmia ( ) Visuaalsed hallutsinatsioonid ( ) ( )( ) EFNS/MDS-ES Parkinsoni tõve diagnostikast Kliiniline diagnostika B tase Geneetiline diagnostika B tase Autonoomse funktsiooni testid vähene tõendus Olfaktoorne test Atüüpiline ja sekundaarne parkinsonism A tase Retsessiivne parkinsonitõbi A-tase Ravimtest ei ole soovitatud parkinsonihaiguse differentsiaaldiagnostikaks Neurofüsioloogilised testid vähe tõenduspõhiseid uuringuid Neuropsühholoogilised testid A tase Neuroradioloogilised uuringud TCS A tase MRI A, B ja C tase SPECT A tase PET vähene tõendus 7
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