Patofisiologi parkinsonism pasca trauma kepala
Wahyu Dwi Hantoro(1*), Indarwati Setyaningsih(2), Mochammad Was’an(3)
(1) KSM Saraf RSI Jakarta Cempaka Putih, Jakarta
(2) Departemen Neurologi Fakultas Kedokteran, Kesehatan Masyarakat dan Keperawatan, Universitas Gadjah Mada, Yogyakarta
(3) Departemen Neurologi Fakultas Kedokteran, Kesehatan Masyarakat dan Keperawatan, Universitas Gadjah Mada, Yogyakarta
(*) Corresponding Author
Abstract
Parkinsonism adalah sebuah sindrom yang ditandai dengan kombinasi dari beberapa gejala kardinal seperti tremor istirahat, rigiditas, bradikinesia, hilangnya refleks postural, sikap tubuh fleksi, dan blocking sistem motorik yang terjadi karena penurunan kadar dopamin akibat degenerasi kerusakan substansia nigra pars kompakta dan saraf dopaminergik nigrostriatum.
Parkinsonisme umumnya bersifat idiopatik yang dikenal sebagai Penyakit Parkinson selain itu juga dapat disebabkan karena mekanisme lain seperti akibat proses infeksi, proses imunulogi, dan sindroma paraneoplastik, penggunaan obat tertentu, paparan toksin, proses vaskular, proses trauma, dan lain-lain. Proses ini yang dikenal sebagai parkinsonism sekunder.
Beberapa penelitian epidemiologi memang telah membuktikan adanya keterkaitan ini tetapi terdapat beberapa penelitian lain yang justru menolak adanya keterkaitan antara trauma kepala dengan kejadian parkinsonism.
Kriteria sebuah trauma kepala berpotensi menimbulkan parkinsonism menurut Crouzon harus memenuhi kriteria antara lain trauma cukup bermakna untuk menyebabkan terjadinya kerusakan pada jaringan otak, waktu proses trauma dengan mulai munculnya gejala parkinson harus jelas, progresivitas gejala neurologis yang nyata, dan derajat keparahan cedera kepala memenuhi kriteria commotio cerebri.
Tinjauan pustaka ini bertujuan mengkaji literatur lebih dalam tentang aspek patofisiologi dari kondisi parkinsonism pasca trauma kepala. Sebagai simpulan patofisiologi dari parkinsonism pasca trauma kepala meliputi degenerasi progresif neuron dopaminergik yang disebabkan terjadinya ekspresi berlebih dan akibat akumulasi α-synuclein dan keterlibatan proses genetik adanya kecacatan pada ubiquitin proteasome system (UPS).
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Kelompok Studi Gangguan Gerak PERDOSSI. Konsensus Tatalaksana Penyakit Parkinson. Jakarta: Desantara Utama; 2003.
Schoutton JW. Neuroprotection in traumatic Brain Injury; A complex struggle against the biology of nature. 2011. Available from: www.ncbi.nlm.nih.gov/pubmed/17327733.
Nader A, Azami M, Jasemi M, Nader SE. Epidemiology of Traumatic Brain Injury in Urmia Iran. Iranian Red Crescent Medical Journal. 2013;15(2):173-174.
Retnaningsih. Cedera Kepala Traumatik. 2008. Available from: http://www.kabarindonesia.com/beritaprint.php?id=20080427234109.
Harris MA, Shen H, Marion S. Head Injury and Parkinson’s Disease in case control Study. Occup Environ Med. 2013;70:839-844.
Dick FD, De Palma G, Ahmadi A, Scott NW, and Felice A. Environmental Risk Factors for Parkinson’s Disease and Parkinsonism: The Geoparkinson Study. 2007. Available from: www.ncbi.nlm.nih.gov/pubmed/17332139.
Goldman SM, Tanner CM, Oakes D, Bhudhikanok GS, Gupta A, Langston JW. Head injury and Parkinson’s disease risk in twins. Ann Neurology. 2012;60:65-72.
Sullivan M. Traumatic Brain Injury Increases risk of Parkinson Disease. 2011. Available from: www.newsroom.ucla.edu/releases/traumatic-brain-injury-a-threat-213647.
Husni A. Penyakit Parkinson, Patofisiologi, Diagnosis, dan Wacana Terapi. Disampaikan pada Temu Ilmiah Nasional I dan Konferensi Kerja III PERGEMI. Semarang: Badan Penerbit Universitas Diponegoro; 2002.
PERDOSSI. Konsensus Nasional Penanganan Trauma Kapitis dan Trauma Spinalis. Jakarta: Prikarsa Utama; 2006.
Weiner M, Veitch DP, Hayes J, Neylan T, Grafman J, Aisen PS, et al. Effects of traumatic brain injury and posttraumatic stress disorder on Alzheimer’s disease in veterans, using the Alzheimer’s Disease NeuroimagingInitiative. The Journal of The Alzheimer’s Association. 2014;10(3):S226–S235.
Glover LE, Tajiri N, Lau T, Kaneko Y, van Loveren H, Borlongan CV. Immediate, butnot delayed, microsurgical skull reconstruction exacerbates brain damage in experimental traumatic brain injury model. PloS One. 2012;7:e33646.
Oh Irene. Movement Disorders in Brain Injury:Neurology, Movement Disorders.The Neurology Center of Southern California. 2013. Available from: https://www.scripps.org/assets/documents/34a_movement_disorders_oh.pdf.
Wan OW, Chung KK. The role of alpha-synuclein oligomerization and aggregation in cellular and animal models of Parkinson’s disease. PLoS One. 2012.7;e38545.
Ulusoy A, Di Monte DA. Alpha-synuclein elevation in human neurodegenerative diseases: Experimental, pathogenetic, and therapeutic implications. Mol Neurobiol. 2013;47:484–494.
Chaudhuri KR, Healy DG, Schapira AH. Non-motor symptoms of Parkinson’s disease: Diagnosis and Management. Lancet Neurol. 2006;5:235–245.
Jankovic J. Parkinson’s disease: Clinical features and diagnosis. J Neurol Neurosurg Psychiatr. 2008;79:368–376.
Goedert M. Alpha-synuclein and neurodegenerative diseases. Nat Rev Neurosci. 2001;2:492–501.
Wakabayashi K, Tanji K, Mori F, Takahashi H. The Lewy body in Parkinson’s disease: Molecules implicated in the formation and degradation of alpha-synuclein aggregates. Neuropathology. 2007;27:494–506.
Klein C, Westenberger A. Genetics of Parkinson’s disease. Cold Spring Harbor Perspect Med. 2012. Available from: www.ncbi.nlm.nih.gov/pubmed/22315721.
Shahaduzzaman Md, Acosta S, Bickford PC, Borlongan CV. α-Synuclein is a pathological link and therapeutic target for Parkinson’s disease and traumatic brain injury. Med Hypotheses. 2013;81:675–680.
Rodrigues TM, Jeronimo-Santos A, Outeiro TF, Sebastiao AM, Diogenes MJ. Challenges and promises in the development of neurotrophic factor-based therapies for Parkinson’s disease. Drugs Aging. 2014;31:239–236.
Conway KA, Lee SJ, Rochet JC, Ding TT, Williamson RE, Lansbury PT, Jr. Acceleration of oligomerization, not fibrillization, is a shared property of both alpha synuclein mutations linked to early-onset Parkinson’s disease: Implications for pathogenesis and therapy. Proc Natl Acad Sci USA. 2000;97:571–576.
Li L, Lih-Shen C. Impairment Of The Ubiquitin-Proteasome System: A Common Pathogenic Mechanism In Neurodegenerative Disorders. New York: Nova Science Inc. Publishers; 2007;p.553-577.
Paine MG, Wooten MW. The Role of the Ubiquitin-Proteasome System and p62 in the Development of Neurogenerative Disease.Impuls: The Premier Journal for Undergraduate Publications in Neurosciences; 2006.
Moore EL. Mild Traumatic Brain Injury and Anxiety Sequele: A Review Of The Literature. Lincoln: Department of Psychology University of Nebraska; 2005.
DOI: https://doi.org/10.22146/bns.v18i2.54995
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