Neurológiai és pszichiátriai betegségek modellezési lehetőségei. a számitógépes idegtudományban. Szalisznyó Krisztina. KFKI RMKI, Biofizikai Osztály

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1 Neurológiai és pszichiátriai betegségek modellezési lehetőségei a számitógépes idegtudományban. Szalisznyó Krisztina KFKI RMKI, Biofizikai Osztály H-1525 P.O. Box 49, Budapest, december 12.

2 1. Könyvajánló Epilepsy as a Dynamic Disease, Series: Biological and Medical Physics, Biomedical Engineering Edited by: Milton John; Jung Peter (Springer) Disorders of Brain, Behaivor and Cognition: The neurocomputational Perspective Edited by: J.A. Reggia, E. Ruppin, D.L.Glanzman (Elsevier) Neurológia Szirmai Imre (Medicina) 1

3 2. Tárgyalt betegségek Epilepszia Bazális ganglionok betegségei (Parkinson betegség, Huntington Chorea) Alzheimer kór Skizophrénia Hangulati zavarok, depresszió és szorongás 2

4 3. Epilepszia Epilepsziák osztályozása, (híres emberek epilepsziával) Etiológia Modellezés és elméleti megfontolások lehetőségei Sejt, hálózat, populáció szintű modellek 3

5 4. Híres emberek epilepsziával Muzsikusok, zeneszerzők, George Frederick Handel - Hector Berlioz - Neil Young Nicolo Paganini - Peter Tchaikovsky - Robert Schumann Írók, költők, filozófusok Blaise Pascal - Charles Dickens - Dante - Edgar Allen Poe - Fyodor Dostoyevsky - Gustave Flaubert - Guy de Maupassant - Lewis Carrol - Lord Byron Professor Manning Clarke - Pythagoras - Sir Walter Scott - Socrates - Truman Capote - Agatha Christie Államférfiak, Alexander the Great - Alfred the Great - Charles V of Spain - James Madison Julius Caesar - Louis XIII of France - Napoleon Bonaparte - Paul I of Russia Peter the great Természettudósok, Alfred Nobel - Pythagoras - Sir Isaac Newton Mások, Aristotle - Hannibal - Harriet Tubman(Ran the Underground Railroad to Free Slaves) - William The Third 4

6 5. Epilepsziák felosztása zajlás és eredet szerint idiopathiás szimptómás benignus centrotemporális temporolimbikus benignus occipitális frontális egyéb occipitális parietális gyermekkori absence West-szindróma Juvenilis abscence Lennoux-Gastaut-szindróma Myoclonus epilepszia Progresszív myoclonus ébredési grand mal egyéb 5

7 6. Epilepsziás rohamok nemzetközi felosztása I. parciális rohamok II. Generalizált rohamok A.)simplex parciális rohamok A.) Absence (petit mal) 1.motoros jelenségekkel 1.) csak tudatzavar 2.Somatosenzoros rohamok 2.) Clonusokkal 3.Autonom jelenségekkel 3.) Atóniával 4.Összetett rohamok, motoros, senzoros, pszichés 4.) Tónusos komponensekkel 5.) Automatizmusokkal 6.) Vegetatív komponensekkel 7.) Atípusos absence B. Komplex parciális rohamok B.) Myoclonus rohamok 1. Csak tudatzavarral C.) Clonusos rohamok 2. Gondolkodászavarral D.) Tónusos rohamok 3. Affektív tünetekkel E.) Tónusos-clonusos rohamok 4. Pszichoszenzoros rohamok F.) Atóniás rohamok 5. Psychomotoros jelenségek 6.Komplex rohamok (fentiek társulásával) C. Parciális rohamok szekunder generalizációval Nem osztályozható rohamok 6

8 7. Epilepsziák etiológiája Channelophatiák: csatornák szerkezeti vagy funkcionális megváltozása Szinapszisok szerkezeti illetve eloszlásbeli változása Extracelluláris ionkoncentráció szabályozási zavara Serkentő és gátló neurotranszmitterek egyensúlyának változása a termelődés, a kibocsátás, lebomlás és visszavételi mechanizmusok zavara miatt. Posztszinaptikus membránon levő neurotranszmitter-receptorok mennyiségi, szerkezeti és funkcionális károsodása Hálózati szintű átstruktúrálódás 7

9 (Prof. Jeffrey Noebels anyaga) 8

10 9

11 8. Hyperexcitabilitás sejtszintű modelljei Öröklött channelophátiák Mutációk, amelyek epilepsziához köthetők. Szerzett channelophatiák downstream channelophatiák, (gyógyszerrezisztencia) Megválaszolatlan kérdések (például): 1.) diverz rohamtípusok 2.) mi kontrolállja a delayed onset epilepsziát 10

12 9. Példák Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder, Nature Genetics, Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy C. Bernard, A. Anderson, A. Becker, N. P. Poolos, H. Beck, D. Johnston Science Persistently modified h-channels after complex febrile seizures convert the seizure-induced enhancement of inhibition to hyperexcitability. Chen K, Aradi I, Thon N, Eghbal-Ahmadi M, Baram TZ, Soltész I. Nature Medicine,

13 10. Kishálózatok Szinaptikus potenciálok változása (K + és Cl ekvilibrium potenciál), (Nerst és Goldman egyenletek eltolódása) Spreading depression Szinaptikus sprouting, kindling Szinapszisok variabilitása és hálózati stabilitás 12

14 11. Bazális ganglionok betegségei Parkinson kór és szindróma Etiológia: Parkinson kór (és skizophrénia) dopamin modellje Modellezés és elméleti megfontolások lehetőségei Sejtszintű modellek, bistabilitás és munkamemória Hálózat szintű modellek 13

15 12. Bazális ganglionok leggyakoribb betegségei (korábbi európai nómenklatúra: exrapiramidális rendszer) Parkinson kór (1817.) An essay on Shaking Palsy, James Parkinson Kórtan: A substantia nigra, a nigrostriatális rendszer, raphe magok, a nucl. basalis Meyert, a locus couruleus és a vágus motoros magjának degenerációja Kémiai változás: Csökken a dopamin mennyisége a striátumban, és a szerotonin norepinephrin rendszer is érintett. Klinikai tünetek: Progresszív neurológiai betegség, 3-5 százalékban az első fokú rokon is beteg. Átlagos betegségkezdet 58 év. Tünetek: rigor, akinézis, bradykinézis, főként nyugalmi tremor, fogaskeréktünet, tartási instabilitás Kezelés: L dopa dekarboxilázgátlóval 14

16 13. Tünettan Hypo/ v. Akinesis Mimikai és szinergiás mozgások készlete szegényedik Marche á petit pas, csoszogó, apró léptű járás Start hesitation, freezing, elindulás és fordulás nehézségei. Tervezett mozgás és beszéd meglassul Fogaskeréktünet (rigor), fej lassan süllyed hátra Nyugalmi tremor, mozgásintenciókor csökkent Tartási és beállítási reflexek, Mentális hanyatlását nem éli meg, executív zavar, munkamemória csökken 15

17 16

18 14. Parkinson-kór részletesebb pathomechanizmusa I.: RIGOR Biokémiai változások Első klinikai tünetek megjelenéséig a striátum elveszítheti dopamintartalmának 70 százalékát!!! Csökken a noradrenalin termelés (loecus ceruleus károsodás) Csökken a szerotonin szint is (raphe magok sérülése) Gátló hátású DA hiánya miatt acetil-kolin túlsúly a striátumban SN pars compactájának dopamin hiánya a D2 receptorokon keresztül (INDIREKT pálya) felfüggeszti a nucleus subthalamicus GABA által mediált gátlását, ezért a gátló hatású globus pallidus (GPi) működése fokozódik, amely GABA-erg gátlás alatt tartja a thalamust. Ugyanilyen hatású a D1 receptorok aktivitásának csökkenése: (a DI- REKT pályán) keresztül a striátum a GPi-t nem tudja gátolni, ezért a talamus a gátlás alól nem szabadul fel, és a mozgatókéreg aktiviása nem jön létre. 17

19 15. Parkinson-kór részletesebb pathomechanizmusa II.: TREMOR Biokémiai változások (lásd előbb) Előbbi séma a tremor létrejöttét nem magyarázza, a nyugalmi tremor ritmusát feltehetően a thalamus azonos frekvenciával tüzelő sejtjei tartják fent. 18

20 Az órán felhasznált képek forrásai: psyc220/kalat/jk246.fig8.15.basal ganglia.jpg ab18bslgang.gif vdbosch/pd.html 19

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26 16. Példák Modulation of striatal single units by expected reward: A spiny neuron model displaying dopamine-induced bistability Aaron J. Gruber, Sara A. Solla, D. James Surmeier, James Houk, Journal of Neurophysiology (2003), Coupled Oscillator Model of the Dopaminergic Neuron of the Substantia Nigra, Wilson CJ and JC Callaway Journal of Neurophysiology (2000), High frequency stimulation of the subthalamic nucleus eliminates pathological thalamic rhythmicity in computational model Rubin JE, Terman D., J. of Computational Neuroscience, 25

27 17. Schizophrénia Dopamin teória > dopamin túlműködés Dopamin és jutalom predikció > addikció tanulása Putámen > motoros striátum Caudátum > centrális és dorzális része szemmozgások, mozgásszervezésben, EXECUTÍV feladatok, munkamemória. Caudátum > ventrális és ventromediális rész, limbikus és prefrontális részekkel, asszociációs striátum 26

28 18. Alzheimer kór senilis neurit plakk, intracelluláris neurofibrilláris köteg acetil-kolin neurotransmisszió zavar I. stádium: entorhinális szakasz (hippokampusz-amygdala rendszer, Schaffer kollaterális rendszer érintettsége, tünetmentesség II. stádium:limbikus szakasz, hippokampusz deafferentálódik, enyhe demencia III. stádium: Isokortikális szakasz, asszociációs kéregben is 27

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