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Mochammad Ridho Nur Hidayah
Abstrak :
ABSTRAK
Pendahuluan: Terbentuknya jaringan fibrosis pada saraf perifer masih menjadi suatu tantangan di bidang orthopaedi terutama dengan eksplorasi saraf. Penggunaan metylprednisolon telah banyak digunakan untuk mengurangi risiko edema jaringan lunak pasca operasi. Penelitian ini bertujuan untuk membuktikan pengaruh pemberian irigasi metylprednisolon asetate terhadap pencegahan perlengketan saraf pada jaringan sekitarnya dan pembentukan jaringan parut epineuralMetode: Dua puluh tikus putih Sprague Dawley jantan yang memenuhi kriteria sampel dibagi ke dalam dua kelompok. Pada seluruh sampel dilakukan perangsangan pembentukan jaringan parut pada saraf skiatika paha kanan menggunakan nylon brush. Kelompok perlakuan diberikan irigasi metylprednisolon asetat 0.1cc; Depomedrol , dan sisanya kontrol. Setelah 4 minggu, tikus dikorbankan, dilakukan pengamatan secara makroskopis dan mikroskopis untuk melakukan perhitungan luas area fibrosis dengan software ImageJ intensifier dan angka Index Fibrotik dengan alat pengukur mikrometer setelah sebelumnya dilakukan pembuatan sedian histologi dengan pewarnaan Haematoksilin Eosin dan Masson rsquo;s Trichrome.Hasil: Terdapat perbedaan yang bermakna antara kelompok perlakuan dan kontrol pada skor Petersen p.
ABSTRACT
Introduction The formation of fibrotic tissue in peripheral nerves is remains a challenge. Methylprednisolone was believed to inhibit fibrotic formation, although its still controversial. This research is intended to prove that the irrigation of methylprednisolone acetate can prevent nerve adhesion on surrounding tissues and the formation of epineural scar.Methods Twenty male Sprague Dawley rats were divided into two groups. Treatment group was irrigated intralesionally with methylprednisolone 0.1cc Depomedrol , and the rest as control. In all samples we performed abrasion injury to stimulate fibrotic formation using nylon brush. The samples were sacrificed after 4 weeks, Peterson score was used to assess macroscopically, and area of fibrotic was measured microscopically. Area of fibrosis was calculated using ImageJ intensifier and fibrotic index number with the micrometer measurement tool after histologic preparation with Haematoxylin Eosin and Masson 39 s Trichrome.Result There was a significant difference between treatment and control group on Petersen score p
2017
T-Pdf
UI - Tesis Membership  Universitas Indonesia Library
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Haznim Fadhli
Abstrak :
ABSTRAK
Latar belakang: Nilai normal Kecepatan Hantar Saraf KHS pada saraf perifer, dipengaruhi oleh faktor-faktor fisiologis, antara lain usia, tinggi badan dan indeks massa tubuh, dan faktor non fisiologis seperti teknik pengukuran dan suhu. Referensi nilai normal tiap laboratorium elektrofisiologi berbeda-beda, sehingga dibutuhkan penelitian untuk memperoleh referensi nilai normal KHS yang sesuai dengan populasi di Indonesia, khususnya di RSUPN dr. Cipto Mangukusumo Jakarta..Metode:Penelitian ini merupakan penelitian prospektif. Responden sehat didapatkan sesuai kriteria inklusi dan eksklusi diambil secara concecutive, usia 18-60 tahun sebanyak 210 subyek. Dilakukan penapisan neuropati perifer dengan wawancara dan kuesioner Brief Peripheral Neuropathy Screening Tool BPNS Tool . Subyek yang memenuhi persyaratan dilakukan pemeriksaan Kecepatan Hantar Saraf KHS motorik dan sensorik pada ekstremitas atas dan bawah, meliputi n.medianus, n.ulnaris, n.radialis, n.peroneus, dan n.suralis. Hasil:Didapatkan sebanyak 210 dari 215 subyek yang memenuhi kriteria inklusi. Subyek penelitian terdiri dari 91 sampel ekstremitas laki-laki dan 119 sampel perempuan. Subjek diambil pada usia dewasa rentang 18-60 tahun, dengan nilai tengah 33 tahun. Subyek terbanyak usia 31-40 tahun, sebanyak 68 sampel 32,4 , jenis kelamin wanita sebanyak 119 sampel 56,7 . Usia subyek dengan nilai tengah 33 22,0-53,4 tahun, dengan tinggi badan subyek 1,6 1,49;1,74 m, dan nilai tengah indeks massa tubuh IMT 24.84 18,5- 31,3 kg/m2.Nilai kecepatan hantar saraf KHS digunakan nilai tengah, dengan batas bawah persentil lima dan batas atas persentil sembilan puluh lima. Nilai KHS motorik pada n.medianus 60 50;73,2 m/det, n.ulnaris 66,6 53;80 m/det, pada n.radialis 67 48,1; 81,8 m/det. n.peroneus 55 39,6;69,8 m/det, n.tibialis 59,5 46,5;75 m/det. Hasil pemeriksaan sensorik, didapatkan KHS sensorik pada n.medianus 66,3 49,6;83 m/det, n.ulnaris 52 41,5;70 m/det, n.radialis 46,7 38,4: 59 m/det. n.peroneus superfisialis 62 44;82 m/det, pada n.suralis 62 48;79 m/det. Kesimpulan:Nilai normal kecepatan hantar saraf motorik pada n.medianus ge;50 m/det, n.ulnaris ge;53 m/det, n.radialis ge;48 m/det, n.peroneus ge;40 m/det, n.tibialis ge;46 m/det. Nilai normal kecepatan hantar saraf KHS pada saraf sensorik pada n.medianus ge; 50 m/det, n.ulnaris ge; 41 m/det, n.radialis ge;38 m/det, n.peroneus superfisialis ge;44 m//det, n.suralis ge;48 m/det.
ABSTRACT<>br> Background The normal value of nerve conduction velocity NCV in peripheral nerves, is influenced by physiological factors, including age, height and body mass index, and non physiological factors such as measurement and temperature techniques. Reference to the normal values of each electrophysiological laboratory is different, so research is needed to obtain references to normal NCV values that are appropriate to the population in Indonesia, especially in dr. Cipto Mangunkusumo Hospital Jakarta. Method This research is a prospective study. Healthy respondents were obtained according to the inclusion and exclusion criteria were taken concecutive, aged 18 60 years as many as 210 subjects.Peripheral neuropathy screening was performed by interview and questionnaire of the Brief Peripheral Neuropathy Screening Tool BPNS Tool . Subjects meeting the requirements were examined for motor and sensory velocity NCV at the upper and lower extremities, including n.medianus, n.ulnaris, n.radialis, n.peroneus, and n.suralis. Result There were 210 out of 215 subjects who met the inclusion criteria. The subjects consisted of 91 samples of male limbs and 119 female samples. Subjects were takenat an adult age range of 18 60 years, with a median of 33 years. Most subjects aged 3140 years, as many as 68 samples 32.4 , gender of women as much as 119 samples 56.7 . Age of subjects with a mean of 33 22.0 53.4 years, with a subjectheight of 1.6 1.49, 1.74 m, and a median body mass index IMT of 24.84 18.5 31.3 kg m2.The value of nerve conduction velocity NCV is used in the middle value, with thelower limit of the fiveth percentile and the upper limit of the ninety five percentile.The value of motor KHS at n.medianus 60 50 73,2 m s, n.ulnaris 66.6 53 80 m s, on n.radialis 67 48,1,81,8 m det. n.peroneus 55 39,6,69,8 m s, n.tibialis 59,5 46,5,75 m s. The results of sensory examination, obtained sensory KHS atn.medianus 66.3 49.6 83 m s, n.ulnaris 52 41,5 70 m s, n.radialis 46,7 38.4 59 m s. n.peroneus superfisialis 62 44 82 m s, on n.suralis 62 48 79 m s. Conclusion The normal value of motor neural conduction velocity in n.medianus ge 50 m s, n.ulnaris ge 53 m s, n.radialis ge 48 m s, n.peroneus ge 40 m s, n.tibialis 46 m s. In the sensory nerves is obtained nerve velocity n.medianus ge 50 .m s, n.ulnaris ge 41 m s, n.radialis ge 38 m s, n.peroneus superfisialis ge 44 m s, n.suralis ge 48 m s.
2017
SP-Pdf
UI - Tugas Akhir  Universitas Indonesia Library
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Australia: Harwood Academic, 2000
616.804 7 DEG
Buku Teks  Universitas Indonesia Library
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Abstrak :
As age related diseases increase in prevalence and impact more significantly on medical resources it is imperative to understand these diseases and the mechanisms behind their progression. New research has stimulated a growing interest in mitochondrial involvement in neurodegenerative disorders such as parkinson’s disease, alzheimer’s disease and multiple sclerosis and the mechanisms which lead from mitochondrial dysfunction to neurodegeneration. Mitochondrial dysfunction in neurodegenerative disorders brings together contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of these diseases, guiding the reader through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, to the consequences of this dysfunction on neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets.
London : Springer, 2012
e20426197
eBooks  Universitas Indonesia Library