Maladia de Parkinson

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Un schizzo per Sir William Richard Gowers de persona affectate per le maladia de Parkinson.

Maladia de Parkinson[1] es un degenerative disordine del systema nervose central affectante principalmente le systema motor.

In paises industrialisate, su prevalentia es de 1% del personas de plus de 60 annos e de 4% del personas de plus de 80 annos.[2]

Signos e symptomas[modificar | modificar fonte]

Symptomas apparece gradualmente, generalmente post le etate de 50 annos: tremores, rigiditate, lentor del movimentos, difficultate pro ambular.[3][4] Le persona affectate pote devenir paralysate. Hypersalivation e dysphagia (difficultate pro deglutir) es alsi signalate[5]. Nonmotor symptomas apparece con le pejoramento del morbo.[3][6] Istos include symptomas olfactive, cognitive, comportamental, de somno o sensorial.[3][7][8] Dementia es commun in stadios avantiate del morbo.

Hallucinationes minor, como le sensation de haber alicuno detra se (hallucination de presentia), serea un symptoma predictive del declino cognitive.[9][10] Epilepsia e perdita auditive pote esser observate usque 10 annos ante le diagnose.[11]

Diagnose[modificar | modificar fonte]

Le morbo es generalmente diagnosticate post le apparition del prime symptomas. Signos precursor pote esser le fatigabilitate e la difficultates de concentration.[12] Dysphagia, gastroparese, syndroma de intestino irritabile sin diarrhea e constipation poterea esser predictive.[13] Diminutiones de spissor del jacimento plexiforme interne del cellulas ganglionar (GCIPL) e del jacimento nuclear interne (INL) del retina pote esser observate in tomographia de coherentia optic (OCL) usque 7 annos ante le diagnose.[14]

Recercatores labora pro identificar biomarkatores permittente un diagnose precoce del morbo per un simple examine de sanguine (es). Alpha-synucleina[15] o pyruvato[16] poterea esser candidatos. Plasmic ratio de DOPA decarboxylase augmenta in patientes suffrente de un carentia de dopamina e poterea contribuer al diagnose precoce del maladia.[17]

Pathophysiologia[modificar | modificar fonte]

Le symptomas motore del morbo resulta del morte de nerval cellulas in le substantia nigre (parte compacte), un region del cerebro medie qui forni dopamina (un neurotransmissor) al basal gangliones.[3] Le causa de iste morte cellular es mal comprendite, sed implicarea le aggregation de alpha-synucleina, constituente corpores de Lewy al interior del neurones.[18][6]

In maladia de Parkinson, proteinas alpha-synucleina deveni mal plicate e se aggrega con altere alpha-synucleinas. Cellulas non pote eliminar iste aggregatos e se damnifica.[18] Le perta de neuron es accompaniate del morte de astrocytos e de un augmentation del numero de microglia in le substantia nigre.[19] Le symptomas comencia quando le parte compacte del substantia nigre es affectate.[20]

Cinque major vias liga basal gangliones al altere cerebral areas. Iste vias son le circuitos motor, oculomotor, associative, limbic e orbitofrontal.[21] Le morbo affecta tote iste circuitos e affecta movimentos, attention e apprentissage, le melio studiate essente le circuito motore.[21]

Se pensa que basal gangliones exerce un rolo inhibitori sur multe systemas motore, impediente inappropriate movimentos. Le dopamina age facilitante le relaxamento del inhibition. In le maladia de Parkinson, le nivello de dopamina diminue e assi, ulle movimento es plus difficile a mandar, ducente al hypokinesia (reduction del movimentos).[21]

Medicamentos usate pro compensar dopamina depletion, inversemente, pote facilitater inappropriate movimentos, producente dyskinesia.[21]

Mitochondrial ADN[modificar | modificar fonte]

Le damnification del ADN del mitochondrios poterea esser implicate in le pathophysiologia.[22]

Etiologia[modificar | modificar fonte]

Le causas del morbo non es cognoscite, sed un combination de factores genetic e ambiental es suspectate.[6] Le risco de cader malade es plus grande si un membro del familia es ja malade, alicun alleles essente cognoscite como factor de risco.[23]

Risco ambiental include expositon al pesticidos e prior trauma al capite; recurrente exposition al trichloroethyleno es alsi suspectate.[24] Al contrario, caffeina e nicotina pare protective.[25][6][26]

Tractamento[modificar | modificar fonte]

Il non ha remedio, sed multes usa L-dopa medicamento.

Referentias[modificar fonte]

  1. ↑ Derivation: Entitates: 1. (it) Malattia di Parkinson || 2. (es) Enfermedad de Parkinson || (pt) Doença de Parkinson || 3. (fr) Maladie de Parkinson || 4. (en) Parkinson's disease || Controlo: (de) Parkinson-Krankheit || (ru) Болезнь Паркинсона || - (Extra): (la) Morbus Parkinsonianus
  2. ↑ de Lau LM, Breteler MM (June 2006). "Epidemiology of Parkinson's disease". The Lancet. Neurology 5 (6): 525–535. doi:10.1016/S1474-4422(06)70471-9. PMID 16713924. 
  3. ↑ 3,0 3,1 3,2 3,3 Parkinson's Disease Information Page (30 June 2016).
  4. ↑ Samii A, Nutt JG, Ransom BR (May 2004). "Parkinson's disease". Lancet 363 (9423): 1783–1793. doi:10.1016/S0140-6736(04)16305-8. PMID 15172778. 
  5. ↑ https://www.marieclaire.fr/maladie-de-parkinson-symptomes,1437569.asp
  6. ↑ 6,0 6,1 6,2 6,3 Kalia LV, Lang AE (August 2015). "Parkinson's disease". Lancet 386 (9996): 896–912. doi:10.1016/s0140-6736(14)61393-3. PMID 25904081. 
  7. ↑ "Psychiatric Manifestation in Patients with Parkinson's Disease" (November 2018). Journal of Korean Medical Science 33 (47): e300. doi:10.3346/jkms.2018.33.e300. PMID 30450025. 
  8. ↑ "The clinical symptoms of Parkinson's disease" (October 2016). Journal of Neurochemistry 139 (Suppl 1): 318–324. doi:10.1111/jnc.13691. PMID 27401947. 
  9. ↑ Alexandra Bresson (2023-06-30). Cette sensation désagréable pourrait être un signe avant-coureur de la maladie de Parkinson, alerte une étude (francese). Version Femina.
  10. ↑ Bernasconi, F., Pagonabarraga, J., Bejr-Kasem, H. et al. (2023-06-29). "Theta oscillations and minor hallucinations in Parkinson’s disease reveal decrease in frontal lobe functions and later cognitive decline" (in en). Nature Mental Health. doi:10.1038/s44220-023-00080-6. 
  11. ↑ doi:10.1001/jamaneurol.2022.0003
  12. ↑ Archive copy. Archivo del original create le 2023-07-04. Recuperate le 2023-07-04.
  13. ↑ Bo Konings, Luisa Villatoro, Jef Van den Eynde, Guillermo Barahona, Robert Burns4, Megan McKnight, Ken Hui, Gayane Yenokyan, Jan Tack & Pankaj Jay Pasricha (2023-07-12). "Gastrointestinal syndromes preceding a diagnosis of Parkinson’s disease: testing Braak’s hypothesis using a nationwide database for comparison with Alzheimer’s disease and cerebrovascular diseases". Gut. doi:10.1136/gutjnl-2023-329685. 
  14. ↑ Siegfried Karl Wagner, David Romero-Bascones, Mario Cortina-Borja, Dominic J Williamson, Robbert R Struyven, Yukun Zhou, Salil Patel, Rimona S Weil, Chrystalina A Antoniades, Eric J Topol, Edward Korot, Paul J Foster, Konstantinos Balaskas, Unai Ayala, Maitane Barrenechea, Iñigo Gabilondo, Anthony HV Schapira, Anthony P Khawaja, Praveen J Patel, Jugnoo S Rahi, Alastair K Denniston, Axel Petzold & Pearse Andrew Keane (2023-08-21). "Retinal Optical Coherence Tomography Features Associated With Incident and Prevalent Parkinson Disease". Neurology. doi:10.1212/WNL.0000000000207727. 
  15. ↑ https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(23)00109-6/fulltext
  16. ↑ https://www.inserm.fr/actualite/une-prise-de-sang-pour-diagnostiquer-precocement-la-maladie-de-parkinson/
  17. ↑ https://www.pourquoidocteur.fr/Articles/Question-d-actu/44985-Maladie-Parkinson-biomarqueur-sanguin-permet-de-l-identifier
  18. ↑ 18,0 18,1 Villar-Piqué A, Lopes da Fonseca T, Outeiro TF (October 2016). "Structure, function and toxicity of alpha-synuclein: the Bermuda triangle in synucleinopathies". Journal of Neurochemistry 139 (Suppl 1): 240–255. doi:10.1111/jnc.13249. PMID 26190401. 
  19. ↑ (2007) "Neuropathology of movement disorders", Parkinson's disease and movement disorders. Hagerstown, MD: Lippincott Williams & Wilkins, 271–283. ISBN 978-0-7817-7881-7. 
  20. ↑ "Diagnosis and Treatment of Parkinson Disease: A Review" (February 2020). JAMA 323 (6): 548–560. doi:10.1001/jama.2019.22360. PMID 32044947. 
  21. ↑ 21,0 21,1 21,2 21,3 "Functional organization of the basal ganglia: therapeutic implications for Parkinson's disease" (2008). Movement Disorders 23 (Suppl 3): S548–S559. doi:10.1002/mds.22062. PMID 18781672. 
  22. ↑ doi:10.1038/s41380-023-02251-4
  23. ↑ Quadri M, Mandemakers W, Grochowska MM, Masius R, Geut H, Fabrizio E, Breedveld GJ, Kuipers D, Minneboo M, Vergouw LJ, Carreras Mascaro A, Yonova-Doing E, Simons E, Zhao T, Di Fonzo AB, Chang HC, Parchi P, Melis M, Correia Guedes L, Criscuolo C, Thomas A, Brouwer RW, Heijsman D, Ingrassia AM, Calandra Buonaura G, Rood JP, Capellari S, Rozemuller AJ, Sarchioto M, Fen Chien H, Vanacore N, Olgiati S, Wu-Chou YH, Yeh TH, Boon AJ, Hoogers SE, Ghazvini M, IJpma AS, van IJcken WF, Onofrj M, Barone P, Nicholl DJ, Puschmann A, De Mari M, Kievit AJ, Barbosa E, De Michele G, Majoor-Krakauer D, van Swieten JC, de Jong FJ, Ferreira JJ, Cossu G, Lu CS, Meco G, Cortelli P, van de Berg WD, Bonifati V (July 2018). "LRP10 genetic variants in familial Parkinson's disease and dementia with Lewy bodies: a genome-wide linkage and sequencing study". The Lancet. Neurology 17 (7): 597–608. doi:10.1016/s1474-4422(18)30179-0. PMID 29887161. 
  24. ↑ "Trichloroethylene: An Invisible Cause of Parkinson's Disease?" (2023). J Parkinsons Dis 13 (2): 203–218. doi:10.3233/JPD-225047. PMID 36938742. 
  25. ↑ (2021) Robbins and Cotran Pathologic Basis of Disease, 10th. 
  26. ↑ "Parkinson's disease and tea: a quantitative review" (February 2009). Journal of the American College of Nutrition 28 (1): 1–6. doi:10.1080/07315724.2009.10719754. PMID 19571153. 

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