Patofisiologi parkinsonism pasca trauma kepala
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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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