Author Archives: driwancybermuseum

The old Thailand Gambling Token Coins

MUSEUM DUNIA MAYA DR IWAN

 S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

THE OLD THAILAND GAMBLING TOKEN COINS  

5

 6

A group of 51 porcelain coins, Thailand for the Chinese aristocracy, 19th century 

Glazed porcelain with stamped and/or underglaze inscription. Divers sizes.

Note: Cf. Vgl. Henry Alexander Ramsden (1872-1915), Siamese Porcelain and other Token , published 1911

Sejarah Tjong A Fie Medan(the History Of Chinese Overseas Captain Medan Tjong a Fie)

SEJARAH TJONG A FIE

Tjong A fie

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

THE HISTORY OF TJONG A FIE

SEJARAH Tjong A Fie

Sejarah Mansion A Tjong A Fie

Tjong A fie Medan
Sebuah rumah yang menonjol yang terletak di jantung Kota Medan di Kesawan Square, rumah yang indah penuh dengan karakter dan budaya belakang sejarah di Medan.

Sejarah Tjong A Fie

Tjong A fie

Tjong Fung Nam, lahir dari keluarga Hakka dan lebih dikenal sebagai Tjong A Fie lahir pada 1860 di desa Sungkow, Moyan atau Meixien. Ia dibesarkan dari sebuah rumah sederhana, dengan kakaknya, Tjong Yong Hian. Keduanya harus menyerahkan sekolah dari usia muda untuk membantu ayah mereka di tokonya. Bahkan dengan pendidikan yang terbatas, Tjong A Fie Cepat belajar keterampilan bisnis dan perdagangan dan segera mengejar mimpi-mimpinya untuk Menjadi Independen dan Sukses, Oleh karena meninggalkan desanya dalam mencari kehidupan yang lebih baik.

Tjong A fie Medan1

Tjong A Fie

Pada tahun 1880, setelah berlayar selama berbulan-bulan, ia akhirnya tiba di pelabuhan Deli (Medan). Itu waktu di Tjong Yong saudaranya Hian Apakah sudah tinggal di Sumatera selama lima tahun dan telah menjadi seorang pedagang dihormati di Sumatera. Namun, Tjong A Fie independen ingin mencari hidup sendiri dan pergi tentang menemukan karyanya sendiri. Tjong A Fie mulai belajar dan mengembangkan keterampilan bisnis dari bekerja untuk Tjong Sui Untuk. Dia mengembangkan keterampilan sosialnya berinteraksi dengan orang-orang dari semua ras, Cina, Melayu, Arab, India, termasuk Belanda. Dia mulai dengan mempelajari bahasa Melayu yang yang Menjadi bahasa nasional yang digunakan di Deli Medan.

Aula Menghibur

Tjong a fie mansion medan1

Tjong A Fie tumbuh dan Menjadi orang yang dihormati di Medan Sumatera, di mana dia tinggal jauh dari judi, alkohol dan Prostitusi di kota Medan berkembang. Dengan rasa yang kuat tentang kepemimpinan dan keadilan, ia Menjadi mediator bagi Cina. Belanda juga mencari Pls bantuannya Perkebunan mereka memiliki masalah dengan isu-isu perburuhan. Kemampuannya untuk memecahkan masalah ini membuatnya mendapatkan Cina untuk Menjadi Mayor. Dengan kinerja yang luar biasa, ia terpilih menjadi Kapten (Kapten).

Para Berbagai kamar

Tjong A fie bedroom

Tjong A Fie dikenal sebagai pengusaha dihormati WHO memiliki jaringan sosial yang baik dan telah membangun hubungan baik dengan Sultan Deli, Al Rasjid Perkasa Alamsjah Makmoen Moeda raja dan tuan. Seperti Mereka Menjadi teman yang baik, Tjong A Fie terpercaya Menjadi pribadi-Nya dan membantu banyak urusan bisnis ditangani.

Tjong A Fie juga Menjadi orang China pertama yang memiliki perkebunan tembakau. Ia juga dikembangkan dan diperluas untuk perkebunan teh di Bandar Baroe dan Besar Kelapa / Palm Perkebunan Kelapa.

Seiring dengan saudaranya Tjong Yong Hian tua, Tjong A Fie mitra joint dengan Tio Tiaw Siat juga dikenal sebagai Chang Pi Shih, pamannya serta Konsulat China di Singapura dan mendirikan sebuah perusahaan kereta api yang dikenal sebagai The Chow-Chow & Swatow Railyway Co.Ltd. di Cina

Ruang Tidur

 

Tjong A Fie, kontributor sosial yang sangat aktif, menyumbangkan sebagian besar kekayaan-bangunannya banyak fasilitas untuk kesejahteraan masyarakat miskin terlepas dari keyakinan ras, kebangsaan atau budaya termasuk banyak tempat ibadah Seperti kuil-kuil Cina & Hindu, Masjid dan Gereja.

Sebagai orang yang dihormati di Medan WHO memiliki banyak Perkebunan, kelapa sawit dan pabrik gula, bank dan perusahaan kereta api, ia mempekerjakan lebih dari 10.000 pekerja. Seperti yang direkomendasikan oleh Sultan Deli, Tjong A Fie diangkat anggota gemeenteraad (dewan kota) dan cultuurraad (budaya dewan)

4 Februari 1921, Tjong A Fie meninggal dari ayan atau perdarahan di otak, di rumahnya di Jalan Kesawan, Medan. Ini Shook kota Medan, Ribuan kawanan untuk membayar hormat dari seluruh termasuk Sumatera Timur, Aceh, Padang, Penang, Malaysia, Singapura dan Jawa. Dia Menjadi legenda dikenal oleh banyak orang di Medan sampai hari ini.

Empat bulan sebelum kematiannya, Tjong A Fie menulis Will di hadapan Notaris Grave Dirk Johan den Facquin.

Side mobil: Mungkin ini nama yang aneh adalah miss-ejaan Kuburan de Fouquain – seperti misalnya ditunjukkan pada Blog Pucca di: Kenangan dari Grave Notaris Nonya Fouquain de – tapi entah cara saya tidak ingin mengucapkan Bahwa nama terkemuka dengan aksen amerika .

Ditulis dalam surat wasiatnya, ia ingin semua kekayaannya untuk dikelola oleh Yayasan Toen Moek Tong tersebut yang didirikan di Medan dan Sungkow pada saat kematiannya. Foundation, yang berbasis di Medan telah diberikan lima misi. Tiga dari Mereka adalah untuk Memberikan bantuan keuangan kepada Orang muda berbakat yang ingin menyelesaikan pendidikan mereka, tanpa ada pilihan budaya atau ras. Foundation juga akan membantu para penyandang cacat yang mampu untuk bekerja tidak lagi termasuk Buta atau Mereka dengan penyakit yang fatal. Ketiga, Yayasan juga Akan Membantu Korban bencana alam dari setiap ras atau kebangsaan.

1873-1924 Aturan Sultan Rashid Al Perkasa Alamsyah Ma’mum, “Builder”.
1878-Miao Zhenjun didirikan oleh orang-orang Chaozhou di Tanjung Mulia (antara Titipapan & Labuan)
Guandi 1880-Miao (Guandi, Caishen, Dabogong) didirikan oleh orang-orang Guangdong di Medan (Jl Irian Barat. 2).
Guanyin 1880-gong (Shakyamuni, Guanyin, Dizang-wang) didirikan oleh orang-orang Xinghua di Medan (Jl. Yos Sudarso 46).
1885 Surat kabar pertama “Deli Courant” diterbitkan.
 
Side Catatan: dalam memeriksa web untuk “Deli Courant” Saya DATANG di banyak gerai makanan cepat saji, atau di toko makanan, di mana Mereka melayani “toko makanan” (Belanda untuk makanan lezat), tetapi juga referensi ke Sutan Sharir – sebuah awal Penting indonesian Negarawan – satu itu para pendiri negara pada kenyataannya, WHO Apakah Akar di Padang dan Medan. Apakah ia juga telah menjadi teman saya studi di Leiden Opa Otto University, di mana Mereka Baik hukum dipelajari. Di perjalanan kembali ke Hindia, Sharir membuat perjalanan laut yang panjang sebagai ‘baby sitter’ pro forma pamanku Ernst (alias Paman Kiddie) Opa sejak Otto masih pada membayar Pemerintah dan berhak atas satu ‘hamba’. Dia memilih untuk membantu Sharir temannya sebagai gantinya.
 
Sjahrir: politik dan pengasingan di Indonesia – Hasil Google Books oleh Rudolf Mrazek – 1994 – Biografi & Otobiografi – 526 halaman
128 Pada 1909-1934 Gemeente Medan (Medan: Deli Courant, 1934), yang menyebutkan Deli Itu adalah sedikit seperti Hindia Timur, liar barat: jika Anda Apakah melakukan pembunuhan di Batavia, Anda masih akan disambut di Medan – dan setiap sepatu Belanda merupakan potensi besar bangsawan di Deli. Sharir Saya Disebutkan sebelumnya dalam entri jurnal saya
 
Kita sekarang dapat melanjutkan dengan timeline:

1886 Lapangan Menjadi ibukota Sumatera Utara.
1886 “Witte Societeit” (“klub lebih besar”) didirikan di samping kantor pos. [Lihat di bawah ini foto]

1888 Sultan Deli (Sultan Rashid Al Perkasa Alamsyah Ma’mum) pindah dari Deli Labuan [serangkaian pitcures bawah ini]
 

 
ke Istana Maimun di Medan. [Setelah dua foto eksterior dan interior:]
 
  

1890 Guandi-gong (Guandi) didirikan di Medan (Jl. Pertemburan 81 – Pulo Brayan dekat)
Shoushan 1891-gong (Guanyin) didirikan oleh Fujianese di Deli Labuan
1895-Miao Zhenjun didirikan oleh orang-orang Chaozhou di Titipapan.
Hotel De Boer 1898 dibangun.
1898-1939 Publikasi dari “Post Sumatera De” oleh Joseph Hallermann, seorang Jerman.
1900 Tjong A Fie rumah dibangun.
1906 Tianhou-gong (Mazu Temple) didirikan di Medan (Baru Jl Pandu 2.)
1907 Sultan Masjid ini dibangun [lihat gambar di bawah ini]
 
 

1908 City Hall (Hulswit & Fermont Weltevreden + Ed Cuypers Amsterdam)
1909-1911 Pembangunan kantor pos (Snuyf, arsitek – kepala Ned.Ind.PWD)
1910 Lapangan adalah kota kecil. Penduduk = 17,500.
1910 Javasche Bank (Hulswit & Fermont Weltevreden + Ed Cuypers Amsterdam) [lihat gambar di bawah ini]
 Medan Mosque

 
  

 

1913 Tjong A Fie menyumbangkan menara jam balai kota.
Gerobak ditarik kuda 1917 adalah nara sumber dengan Sapu digunakan untuk membersihkan kota.
1923 Renovasi Balai Kota.
1923 Zhenlian-si (Guangze-zunwang, Yii-dadi) didirikan oleh orang-orang Chaozhou di toko-toko Durian.
1924-1945 Aturan Sultan Amaluddin Al Sani Perkasa Alamsyah
1928 Bermotor kendaraan nara sumber yang digunakan untuk menggantikan kuda mobil untuk membersihkan kota.
1929 Kantor Perusahaan Dagang Belanda (sekarang Bank Exim) telah selesai (digunakan oleh Gunseikanbu Selama pendudukan Jepang).
1936-ting Guanyin (Guanyin) dibangun oleh Hakka perempuan di Medan (Jl. Lahat 54)
1936 Baolian-tang (Guanyin) didirikan oleh perempuan Chaozhou di Medan (Jl. Sun Yat Sen)
Akhir 1942 pemerintahan Belanda. Penduduk = 80.000.
2000 populasi Field = 1.898.013
 
. Cf: Deli Maatschappij – Wikipedia
Deli Maatschappij NV de bedrijf van een adalah Nederlands koloniale oorsprong. Het bedrijf pintu adalah pada tahun 1869 Nienhuys opgericht Yakub als een tabakscultuurmaatschappij Met voor het concessie Sultanaat Deli di Sumatera, Nederlands-Indie. Di Deli Maatschappij voor de 50% geparticipeerd werd pintu de Nederlandsche Handel-Maatschappij. Dalam de eeuw negentiende exploiteerde Deli Maatschappij de 120 000 hektar. De activiteiten vormden Maatschappij voor een van de een impuls sterke groei van de stad Medan. Het toenmalige hoofdkantoor Deli Maatschappij van de di Medan Paleis van het tegenwoordig van de Gouverneur Sumatera.

Terjemahan: Deli Maatschappij NV adalah sebuah perusahaan asal Belanda kolonial. Perusahaan ini didirikan pada tahun 1869 oleh budaya tembakau Nienhuys Yakub sebagai perusahaan dengan konsesi untuk Kesultanan Deli di Sumatera, Hindia Belanda. Di Deli Company ada partisipasi 50% dari Masyarakat Perdagangan Belanda. Pada Abad Kesembilan Belas Deli Company dieksploitasi 120.000 hektar. Kegiatan perusahaan membentuk suatu dorongan untuk pertumbuhan yang kuat dari kota Medan. Markas mantan Deli Company di Medan saat ini istana Gubernur Sumatera. [Lihat foto di bawah ini di sebelah kiri]

 

English Version

 
 
 
 
 
 
 

THE HISTORY OF TJONG A FIE

History of The Tjong A Fie Mansion

A prominent home located in the heart of Medan City at Kesawan Square, this beautiful mansion is full of characters and cultures behind its history in Medan. Tjong A fie Medan

The History of Tjong A Fie

Tjong Fung Nam, born from Hakka family and more popularly known as Tjong A Fie is born on 1860 in the village of Sungkow, Moyan or Meixien.  He was raised from a simple home, with his elder brother Tjong Yong Hian.  Both have to give up schooling from a young age to help their father in his shop.  Even with limited education, Tjong A Fie quickly learned the business and trading skills and soon pursued his dreams to become independent and successful, hence leaving his village in search for a better life.

Tjong A fie

Tjong A fie

In 1880, after sailing for months, he finally arrived at the port of Deli (Medan).  At that time his brother Tjong Yong Hian had already been living in Sumatra for 5 years and had became a respected merchant in Sumatra.  However, the independent Tjong A Fie wanted to find his own living and went about finding his own work.  Tjong A Fie started to learn and develop business skills from working for Tjong Sui Fo. He developed his social skills interacting with people of all races, Chinese, Melayu, Arab, India, including Dutch.  He began by learning the language Bahasa Melayu which became the national language used in Medan Deli.

Tjong A fie Medan1

The Entertaining Hall

Tjong A Fie grew and became a well respected person in Medan Sumatra, where he stayed away from gambling, alcohol and prostitution in the developing town of Medan.  With his strong sense of leadership and fairness, he became the mediator for the Chinese. The Dutch also seek his help when their plantations have problems with labor issues.  His ability to solve these issues earned him to become the Chinese lieutenant. With his outstanding performance, he was elected to become a Captain (Kapiten).

Tjong a fie mansion medan1

The various rooms

Tjong A Fie was known as a respected businessman who has good social networks and has build good relation with the Sultan Deli, Makmoen Al Rasjid Perkasa Alamsjah and Tuanku Raja Moeda.  As they became good friends, Tjong A Fie became his trusted person and helped dealt with many business matters.

Tjong A Fie also became the first Chinese to own a tobacco plantation. He also developed and expanded to tea plantation in Bandar Baroe and large coconut/palm oil plantations.

Along with his elder brother Tjong Yong Hian, Tjong A Fie joint partner with Tio Tiaw Siat also known as Chang Pi Shih, his uncle as well as consulate of China in Singapore and set up a railway company known as The Chow-Chow & Swatow Railyway Co.Ltd. in China

Tjong A fie bedroom

The Bedroom

Tjong A Fie, a very active social contributor, donated much of his wealth building many facilities for the welfare of the poor regardless of race, cultural beliefs or nationality including many places of worships such as Chinese & Hindu temple, Mosques and Churches.

As a well respected person in Medan who owns many plantations, palm oil and sugar factories, banks and railway companies, he employed more than 10.000 workers. As recommended by Sultan Deli, Tjong A Fie was appointed member of gemeenteraad (city council) and cultuurraad (cultural council)

4 February 1921, Tjong A Fie passed away from apopleksia or bleeding in the brain, in his home at Jalan Kesawan, Medan.  It shook the city Medan, thousands flock to pay respect from all over including Sumatera Timur, Aceh, Padang, Penang, Malaysia, Singapore and Java. He became a legend known by many in Medan till today.

Four months before his death, Tjong A Fie wrote his will in the presence of notary Dirk Johan Facquin den Grave.

Side  car: this odd name is probably a miss-spelling of Fouquain de Grave–as for instance shown in Pucca’s Blog: Memories of a Nonya Notaris Fouquain de Grave–but either way I would not want to pronounce that eminent name with an American accent. 

Written in his will, he wanted all his wealth to be managed by Yayasan Toen Moek Tong which was established in Medan and Sungkow at the time of his death. The Yayasan based in Medan has been given 5 missions. Three of them are to provide financial help to young talented people that wished to complete their education, without no cultural or racial choice. Yayasan will also help the disabled who are no longer able to work including the blind or those with fatal illness.  Thirdly, the Yayasan will also help victims of natural disaster of any race or nationality.  

1873-1924 The rule of Sultan Ma’mum Al Rashid Perkasa Alamsyah, “the Builder”.
1878 Zhenjun-miao was erected by Chaozhou people in Tanjung Mulia (between Titipapan & Labuhan)
1880s Guandi-miao (Guandi, Caishen, Dabogong) was erected by Guangdong people in Medan (Jl. Irian Barat 2).
1880s Guanyin-gong (Shakyamuni, Guanyin, Dizang-wang) was erected by Xinghua people in Medan (Jl. Yos Sudarso 46).
1885 The first newspaper “Deli Courant” was published.
 
Side Note: in checking the web for “Deli courant” I came across many fastfood outlets, or deli’s, where they serve “delicatessen” (Dutch for delicacies) but also a reference to Sutan Sharir–an important early Indonesian statesman–one of that country’s founding fathers in fact, who had roots in Padang and Medan. He had also been a study friend of my Opa Otto at Leiden University, where they both studied law. On the way back to the Indies, Sharir made the long ocean trip as the pro forma ‘babysitter’ of my uncle Ernst (aka Oom Kiddie) since Opa Otto was still on Government pay and entitled to one ‘servant’. He opted to help out his friend Sharir instead.
 
Sjahrir: politics and exile in Indonesia – Google Books Result by Rudolf Mrázek – 1994 – Biography & Autobiography – 526 pages
128 In Gemeente Medan 1909-1934 (Medan: Deli Courant, 1934),  which mentions that Deli was a bit like the East Indies wild west: if you had committed murder in Batavia, you’d still be welcome in Medan–and every Dutch loafer was a potential grand seigneur in Deli. I mentioned Sharir before in my journal entry 
 
Now we can continue with the timeline:
1886 Medan became the capital of northern Sumatra.
1886 “Witte Societeit” (“a rather grand club”) was erected next to the post office. [see photo hereunder]
1888 Sultan of Deli (Sultan Ma’mum Al Rashid Perkasa Alamsyah) moved from Labuhan Deli [series of pitcures below]
 
 
to the Maimoon Palace in Medan. [following two photographs of exterior and interior:]
 
 
1890 Guandi-gong (Guandi) was erected in Medan (Jl. Pertemburan 81 – near Pulo Brayan)
1891 Shoushan-gong (Guanyin) was erected by Fujianese in Labuhan Deli
1895 Zhenjun-miao was erected by Chaozhou people in Titipapan.
1898 Hotel De Boer was constructed.
1898-1939 Publication of “De Sumatra Post” by Joseph Hallermann, a German.
1900 Tjong A Fie mansion was built.
1906 Tianhou-gong (Mazu temple) was erected in Medan (Jl. Pandu Baru 2)
1907 Sultan Mosque was built [see pictures below]
 
 Medan Mosque
1908 City Hall (Hulswit & Fermont Weltevreden + Ed Cuypers Amsterdam)
1909-1911 Construction of post office (Snuyf, architect – head of Ned.Ind.PWD)
1910 Medan was a small city. Population = 17,500.
1910 Javasche Bank (Hulswit & Fermont Weltevreden + Ed Cuypers Amsterdam) [see pictures below]
 
 
 
 
1913 Tjong A Fie donated the city hall’s clock tower.
1917 Horse drawn carts with brooms were used for town cleaning.
1923 Renovation of City Hall.
1923 Zhenlian-si (Guangze-zunwang, Yuhuang-dadi) was erected by Chaozhou people in Kedai Durian.
1924-1945 The rule of Sultan Amaluddin Al Sani Perkasa Alamsyah
1928 Motorized vehicles were used to replace the horse drawn cars for town cleaning.
1929 Office of Netherlands Trading Company (now Bank Exim) was completed (used by Gunseikanbu during the Japanese occupation).
1936 Guanyin-ting (Guanyin) was erected by Hakka women in Medan (Jl. Lahat 54)
1936 Baolian-tang (Guanyin) was erected by Chaozhou women in Medan (Jl. Sun Yat Sen)
1942 End of Dutch rule. Population = 80,000.
2000 Medan’s population = 1,898,013
 

De N.V. Deli Maatschappij is een Nederlands bedrijf van koloniale oorsprong. Het bedrijf is in 1869 opgericht door Jacob Nienhuys als tabakscultuurmaatschappij met een concessie voor het Sultanaat Deli in Sumatra, Nederlands-Indië. In de Deli Maatschappij werd voor 50 % geparticipeerd door de Nederlandsche Handel-Maatschappij. In de negentiende eeuw exploiteerde de Deli Maatschappij 120.000 hectare. De activiteiten van de maatschappij vormden een impuls voor een sterke groei van de stad Medan. Het toenmalige hoofdkantoor van de Deli Maatschappij in Medan is tegenwoordig het paleis van de Gouverneur van Sumatra.

Translation: The NV Deli Maatschappij is a Dutch company of colonial origin. The company was founded in 1869 by Jacob Nienhuys as a tabacco culture company with a concession for the Sultanate Deli in Sumatra, Netherlands East Indies. In the Deli Company there was a 50% participation of the Netherlands Trading Society. In the nineteenth century the Deli Company exploited 120,000 hectares. The activities of the company formed an impulse for the strong growth of the city of Medan. The onetime headquarters of the Deli Company in Medan is today the palace of the Governor of Sumatra. [See photo below on the left]

THE END @ copyright Dr Iwan suwandy 2011

The Cute Innocent Expression Art Photography

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

THE CUTE’S INNOCENT EXPRESSION ART PHOTOGRAPHY

part one

I.THE CUTE EURO INNOCENT EXPRESSION

If You want to choose a girlfriend,fiance or Wife,please look rthdeir innocent exprsession like the art photography below.

 

 AND WHEN YOU MET HER,PLEASE SING A LOVE SONG

VISION OF YOU VISION OF BLUE

OR

YOU ARE ALWAYS IN MY HEAT OR PLEASE RELEASE ME AND LET GO IF THEIR EXPRESSION NOT INNOCENT!!!!!!!!!!

II.THE CUTE ASIA INNOCENT EXPRESSION

iF YOU LOOK AT THEIR INNOCENT BODY LANGUAGE,P,LEASE DON’T LET HER GO

 GIVE HER THE ROSE FLOWER WITH DIAMOND RING

ASKED HER

WILL YOU ASCEPT THIS RING

 

SHE SAID WO AI NI

I LOVE YOU

MY LOVE,

WHICH ONE YOU CHOOSE PLEASE TELL ME VIA COMMMENT

the end @ copyright Dr Iwan suwandy 2011

The Singking Of Lampong Poetry about Krakatoa mount eruption 1883

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

The sinking of Lampong poetry
about

The eruption of Mount Krakatau

 

Top of Form

Long before foreign researchers wrote about the eruption of Mount Krakatau (Krakatoa, Carcata) on 26, 27, and August 28, 1883, a native witness has written a very rare and interesting, three months after the eruption of  Krakatoa through Lampung Karang (Lampong sinking) poetry .

 

“Scientific studies and bibiliografi about Krakatoa almost missed include only indigenous written sources, which record the testimonies of the eruption of Krakatoa in 1883. Two years of research, I found the only native testimony in written form, “he said. Before the eruption on 26, 27, and August 28, 1883, the Krakatoa volcano has coughed since May 20, 1883. Krakatoa eruption caused pyroclastic as high as 70 km and 40-meter high tsunami that killed about 36,000 people.


Before the 1883 eruption, Mount Krakatoa had never exploded around the year 1680 / 1.

The eruption that led to the three islands adjacent to each other; Sertung Island, Little Rakata Island, and the island of Rakata. Suryadi explained, as long as it is to be reading about the eruption of Mount Krakatoa is a complete research report GJ Symons et al, The Eruption of Krakatoa and Subsequent Phenomena: Report of the Krakatoa Committee of the Royal Society (London, 1888).

While the indigenous written sources published in Singapore in printed form stones (litography) in 1883/1884. Kolofonnya recorded in 1301 AH (November 1883-October 1884).

 

The first edition is titled Poetry Lampung District Water and Rain ridden by Abu (42 pages). “A short time later came the second edition of this poem with the title This is the poem Lampung ridden Sea (42 pages). The second edition was also published in Singapore on 2 Safar 1302 H (21 November 1884), “he explained.
The third edition of the poem titled Lampung and Anyer and the Cape Coral Sea Rise (49 pages), published by Haji Said. This third edition also published in Singapore, bertarikh 27 Rabiulawal 1301 AH (January 3, 1886). In some ads, this third edition of the poem called Anyer Sunset District. “

The fourth edition of this poem, the last edition as far as I know, This is the poem entitled The Karam Lampung (36 pages). This fourth edition also published in Singapore, Safat bertarikh 10 1306 H (October 16, 1888), “said Suryadi, the dozens of research results have been published in various international journals.
According to Suryadi, the fourth edition of the text special poem written in Malay and Arabic wear-Malay (Jawi). From the comparison of the text which he did, there are significant variations between each edition. This indicates that kelisanan influence is still strong in the tradition of literacy that began to grow in the archipelago in the second half of the 19th century.
Suryadi who managed to identify the place where copies of all editions of Lampung Karam poem that still exists in the world until now to mention, Lampung poem written Karam Mohammed Saleh. He admitted writing the poem in Kampung Bangkahulu (then called Bencoolen Street) in Singapore. “Muhammad Saleh claimed was in Cape Coral when the eruption of Krakatoa occurred and witnessed the great natural disaster that with his own eyes. It is likely that the poet was a victim of the eruption of Krakatoa which went fled to Singapore, and brings scary memories of natural disasters mahadahsyat it, “he said.
 Lampung Karam or the sinking of Lampong poetry can be categorized as a poetic journalism, because the more strongly highlight the nuances of journalism. In Lampung Karam Poetry 38 pages in length and 374 verse, Mohammed Saleh dramatically illustrate the great disaster that followed the eruption of Mount Krakatoa in 1883. He told the destruction of villages and mass death caused by the eruption. Areas such as Earth, Kitambang, Gutters, Kupang, Lampasing, Umbulbatu, Benawang, Rhino, Limes, monkey, Mount Bases, Gunung Sari, Minanga, Tanjung, Kampung teba, Middle Village, Kuala, Rajabasa, Cape Coral, Island also Sebesi , Sebuku, and Peacock devastated by the tsunami, mud, and rain of ash and rock.
The author tells how in a heartbreaking situation and turmoil, people are still willing to help each other help each other. However, not a few who take the opportunity to enrich themselves by taking the property and other people’s money is overwritten disaster. Besides tracing the editions published poem Lampung Karam remaining in the world until now, the study also presents transliterations Suryadi (control characters) text of this poem in the Latin alphabet.

another info

The legendary annihilation in 1883 of the volcano-island of Krakatoa — the name has since become a by-word for a cataclysmic disaster — was followed by an immense tsunami that killed nearly 40,000 people. Beyond the purely physical horrors of an event which has only very recently become properly understood, the eruption changed the world in more ways than could possibly be imagined. Dust swirled round the world for years, causing temperatures to plummet and sunsets to turn vivid with lurid and unsettling displays of lght. The effects of the immense waves were felt as far away as France. Barometers in Bogota and Washington went haywire. Bodies were washed up in Zanzibar. The sound of island’s destruction was heard in Australia and India and on islands thousands of miles away.

 

The 1883 explosion on an uninhabited island in Indonesia was one of the most catastrophic in history. Before the eruption, this island in the Sunda Straits between Java and Sumatra islands was made up of three stratovolcanoes that had grown together.

 


In the summer of 1883, one of Krakatau’s three cones became active. Sailors reported seeing clouds of ash rising from the island. The eruptions reached a peak in August, culminating in a series of tremendous explosions. The most ear-shattering eruption was heard in Australia, more than 2,000 miles (3,200 kilometers) away.

 


Ash was sent 50 miles (80 kilometers) into the sky and blanketed an area of 300,000 square miles (800,000 square kilometers), plunging the area into darkness for two and a half days. The ash drifted around the globe, causing spectacular sunsets and halo effects around the moon and sun.

 

 

The explosions also sent as much as 5 cubic miles (21 cubic kilometers) of rock fragments into the air. The northern two-thirds of the island collapsed under the sea into the newly vacated magma chamber. Much of the remaining island sank into a caldera about 3.8 miles (6 kilometers) across.

The collapse set off an immense series of tsunamis, or giant sea waves, that traveled as far as Hawaii and South America. The largest wave loomed 120 feet (37 meters) high and destroyed 165 nearby settlements. All vegetation was stripped bare, structures were
demolished, and some 30,000 people were washed out to sea in Java and Sumatra.

Krakatau was quiet until the 1920s, when volcanic activity began again. Since then, eruptions have built a new cone, Anak Krakatau, or “child of Krakatau” in the center of the caldera created in 1883

Krakatoa eruption 1930

 

Krakatoa mount now

 

the end @ copyright Dr Iwan Suwandy 2011

The Rare Asia Vintage Postcard Part Two(A_S)

Rare Asia Postcard

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

The  Rare Asia Vintage Postcard Part Two

Rare Asia Postcard Part One

(A-I)

ADEN

 

BURMA(Myanmar)

 

 

 

 

Cambodge

 

 

 

 

Ceylon(Srilanka)

 

 

 

 

 

 

COREA

 

 

 

Indochine-Vietnam

a.Lao Bao

 

b.Quan Yen

 

 

 

c.Yen-Te

 

 

Rare Asia Postcard

(I-Z)

 

IRAN-Persia

 

 

IRAQ-Mesopotamia

British camp

 

ISRAEL

.Jaffa

 

 

Japan

 

 

 

 

 

France consulate Nagasaki

 

 

Japan Occupation

a.Hongkong

 

 

b.Canton China

 

LAOS-Indochine

 

 

 

 

Lebanon

Beyrouth

 

 

MALAYSIA

Kuala lumpur

 
 
 
During the open mining area in the Ampang and Kuala Lumpur, the people who berkelian tin Mandailinglah there, in addition to the furnace, buying tin and business. Bugis kings collect taxes from those who mandailing on the bases of the river.
Even the name “Ampang” itself may be taken in conjunction with the dams built by the mandailing in berkelian tin works. Water used to remove ore from the rock.When Sutan Fasting in Ampang, the son of the king mandailing dealing with Chinese merchants Hiu Siew and his friend Ah Sze Potato from Cobra. Both quarter-Hakka Chinese merchant was then moved to Ampang after being informed by Sutan fast that they can quickly make a profit in Ampang

 
 
mile away from the meeting Sungai Gombak and Sungai Klang as a base for their stores. This occurs in approximately 1859. Mouth of both rivers are then called the Kuala Lumpur – perhaps because of sloppy work in the stomach berkelian tin the rivers.
 

OLD NAMES OF ROADS IN KUALA LUMPUR

Penang

 

Penang

 

batuferringhi

This is Batu Feringhi. Thats Lover’s Isle there in the sea. The beach then was definetly unspoilt and as can be seen, not a hotel in sight.

capitanklingmosque

The famous Mesjid Kapitan Keling. Look at the car, that tells you that this is old.

chuliast

Chulia Street. Funny, even then it looked old. The car tells you its old.

 ferry1958

This is a scene in the ferry. Notice the dressing then. I am told this is taken in 1958.

penang01

I think this is somewhere near Padang Kota Lama. I may be wrong.

 penang07

I am still trying to figure out which place this is. Can anyone help me out here? Hey I am a mainland boy and resides in Penang Island only since 1993 besides the 2 or 3 years in 1984.

penanghillpolisstation

The Penang Hill Police Station. The last time I went up that hill was probably 8 years ago and if I am not mistaken, the police station looked the same.

penanghillview

View of Penang Island from the hill. Lots of changes I tell you.

penangroad1

This is Penang Road of old. Notice one thing in particular? What you asked? Look, no jam.

penangroad2

Penang Road again. Trishaws or Lang Chia or some people like to call it lancheows were the king of the road then. Is that a Lambretta?

penangroad3

The Odeon Cinema. Now it plays only Tamil movies. Look at Rajnikant waiting there and again, no jam.

penangroad5

No jam along Penang Road. I think if you know what year the movie Annastasia was shown, it would help in determing the age of this photo.

penangroadpolisstation

Hey we had double deckers back then. I don’t know if I had ridden in one or not. If I had, I must have been too young to remember so Kerp, don’t go saying you were in one.

tanjongtokong

Besides the double decker, this is another of my favourite. Tanjong Tokong and old Malay huts. This is a classic man.

waterfall

The Botanical Gardens. I remember the excitement of going there and feeding the monkeys. They still do have monkeys now and also two legged ones.

Palestine

 

 

Jerusalem

 

 

PHILLIPINE

 

 

 

SINGAPORE

Native tamasek

 

 

 

SYRIE

 

THAILAND-Siam

 

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The end @ copyright

 Dr Iwan Suwandy 2011

 

The Rare Asia Vintage Postcard Collections Part One:CHINA

Rare Asia Postcard

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

The High Investation Value China  vintage Postcard

 

1.Ethnic Traditional

 

 

 

 

Native people

 

2.City View

a.Tientsin

 

b.Macao

 

 

 

 

 

c.Cancun

 

d.Hankow

 

 

e.Tientsin Museum

 

f.Nanking road

 

 

3.Historic

a.Boxer Rebellion

1)foreign pictures

 

 

2)China Boxer REVOLT Arsenal Hanyang Hupeh Taken

 

3).CHINA BOXER REBEL Arsenal after Capture of SHANGHAI OLD

 

b.Tientsin Massacred

TIENTSIN – PEKING – PEKIN – DECAPITATIONS

 

 

4.Foreign Monument

a.German,America and Japanese Consulate at Shanghai

  

b.Astor Hotel Shanghai

 

c.Hotel La Paix Tientsin

 

d.Russian Cruiser China

 

5.Old China Monument

a.Beijing monument Tu Lien Pagoda used via foreign Postal

 

b.Temple Of Heaven

 

 

c.Ming Tomb

 

d.Harbin Church

 

6.China Old Transportations

a.Tram held by horse

 

b.Imperial TrainTientsin

 

 

c.Sparow Boat

 

d.Rickshaw at Hongkong

 

 

e.Automobile

 

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The end @ copyright

 Dr Iwan Suwandy 2011

The High Investation Value PHONECARD Collections

 

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

rare

uncommon

The High Investation Value Of

PHONE CARD Collections

 

 

INTRODUCTIONS

In Indonesia the rarest local phonecard  collections were the limited promotuional edition KERIS GALERY(issued 300 only )

Keris Gallery (Reverse Side: Silver, Bars On Front)

and Jiffy(issued 400 only),very difficult to found in unused or mint conditions.

The rare International Phonecard very difficult to found in Indonesia, but Dr Iwan Had found three limited editiond phone card from Coca Cola promition

 

and McDonald promotions, especially the proof limited only 28 card only

,

the other 5rare was prepaid phonecard HALO from east Timor

If the co9llectors who found the same card please informed me, and I will show some rare International phonecard found from international Auctions.

Jakarta November 2011

Dr Iwan suwnady

 

I.Dr Iwan Masterpiece Collections

1.COCA COLA PROMOTION

(not list in any auctions)

Coca Cola Sprint Phone Card/Cells Premier Edition

Limited Hot Cel 1 of 610

 

 

 

2.MC DONALD’S PROMOTION

(not list in any auctions)

1)McDonald’s In Tokyo Established 1971

Limited Edition

Proof 26 of 28

2)Mc Donald Happy Meal

,Guys French Fries

Diet Cut

Limited editions

113 of 856

 

3) with this rare card above ,Dr Iwan also found uncommon card

$2.-Card of NBA star profile Charles Barkeley(list in auctions)

  

II.International Masterpiece Collections

1.Proof Snowflakes Trial :

First Edition Debit Card of Ameritech

$1.

 

$5.-

 

 

 

 

2.TAMRA Electric Works Ltd Promotion Test Card

 

a.NewYork City Skyline,Bridge and twin Tower of WTC

b.Diamond Head & Beach

  

3.HAWAIAN TELEPHONE

1).Diamond Head and Waikiki Beach

  

2)Raibow Valley Issued,eclipse Hawaii

July,11,1991 Overprint

 

4.OTHER RARE HAWAII PHONECARDS

1) 10u Coastal Lights & Hawaii at Bottom-Left (Tel Bold)

 

2) 3u Hula Girl By Night (Tel)

  

3) 3u Whales of Hawaii Humpback Whale

  

5.SPORT THEMATIC

1)$49 Jerry Rice 1994

Record breaker 49ers.

   

2) PhonePak 1996 $100. Jeff Gordon (DuPont, McDonalds) # Printers Proof [210 USD]

6.COCA COLA PROMOTION

1)Smith Coke 1994 Grand Prize Winner Santa & Bear Toasting Coca-Cola

 

2 1997 Smith:600 m Woman,Co9ke Bottle &Skis GRAND PRIZE WINNER

 

  

3.1998 Smith : 600 m Woman (Rede Coat) with Skis GRAND PRIZE WINNER

  

7.FAMOUS PERSONS

1)ACTRESS

(1) $3.00 Marlene Dietrich:

a) $3,00,Blue Dress & Large Pendant (by: Watts)

 

b) $6.00 Marlene Dietrich: In Red Dress & Hat (Artist: Perillo) GOLD

 

(2)$50. Marilyn Monroe A

 (In White Strapless Dress)

 

  

2)PRESIDENT

(1)RONALD REAGAN

 

 

(2)NELSON MANDELA

3)POPE

JOHN PAUL II

$10. Purple Pope John Paul II Visit To Denver – Rare Prototype

4)SINGER

Elvis Presley

 

 

 

 

8.COIN$SAVER PROMO

RARE Set of 4 Original Coin$aver JUMBOs (Internal) $5,$10,$50,$100. [8995 USD]

 

 

9.FIRST JUMBO CARD EVER ISSUED

7u Telecard Man JUMBO (AmeriVox): 1st Jumbo Card Ever Issued 9/93 [450 USD]

 

10.MULTIMEDIA DEMONSTRATION CENTER GRAND OPENING

10u Multi-Media Demonstration Center Grand Opening *SAMPLE* [375 USD]

 

11.BACK TO SCHOOL PROMO

$7.50, $15.,$30.,$60. Back To School (4 Card SAMPLE Set) [1100 USD]

 

 MORE INFORMATION ONLY FOR PREMIUM MEMBER,PLEASE SUBSCRIBED VIA COMMENT

 

 

 

THE END

 

 

 

HOLOCARD

 

 

 @copyright Dr Iwan suwandy 2011

 

 

The Rare Albania Handoverpint Eagle Stamps 1913

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

THE RARE ALBANIA

HANDSTAMPED OVERPRINT EAGLE

1913 STAMPS

In 1913 Albania issued a very beautiful and amizing overprint eagle on Turkish Stamps, many Eagle thematic stamps collectors xseeking this stamps. Now the value of the stamps very high espacially postally used on fragment, and until this day I never seen this stamps postally used on Covers,please who have  be kind to show us.

This rare stamps  have three types colours overprint  Black,Violet and Red, I hope the collectors from all over the world will happy to look at this rare stamps and becareful for the fake one.

(Dr Iwan Notes)

THE RARE COLLECTIONS SHOW

1.BLACK OVERPRINT

2.VIOLET OVERPRINT

3.RED OVERPRINT

The history of Alabnia in 1913

Independence of Albania (1912)

The initial sparks of the first Balkan War in 1912 were ignited by the Albanian uprising between 1908 and 1910[43] which were directed at opposing the Young Turk policies of consolidation of the Ottoman Empire. Following the eventual weakening of the Ottoman Empire in the Balkans, Serbia, Greece and Bulgaria declared war and sought to aggrandize their respective boundaries on the remaining territories of the Empire. Albania was thus invaded by Serbia in the north and Greece in the south, restricting the country to only a patch of land around the southern coastal city of Vlora. In 1912 Albania, still under foreign occupation, declared its independence and, with the aid of Austria-Hungary, the Great Powers drew its present borders. The territorial security of Albania was guaranteed by the Great Powers in the Treaty of London of 1913.

The border between Albania and its neighbors was delineated in 1913 following the dissolution of most of the Ottoman Empire’s territories in the Balkans. The delineation of the new state’s borders left a significant number of Albanian communities outside Albania. This population was largely divided between Montenegro and Serbia (which then included what is now Kosovo and the Republic of Macedonia). A substantial number of Albanians thus found themselves under Serbian rule. At the same time, an uprising in the country’s south by local Greeks, led to the formation of the Autonomous Republic of Northern Epirus in the southern provinces (1914). After a period of political instability brought about by the First World War, the country adopted a republican form of government in 1920.[44] The territorial security of Albania was guaranteed by a League of Nations declaration of November 9, 1921, which entrusted the defense of that state to Italy

OTHER ALABANIA RARE STAMPS

1.COMET HANDSTAMPED OVERPRINT

2.MOTHER THERESIA SHEET

the end @ copyright dr Iwan suwandy 2011

Indonesia SEA GAMES 2011

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

INDONESIA SEA GAMES 2001 LIVE NOW

PREPARATION OPENING CEREMONY

11.11.11

 

 LIVE EVENT OPENING CEREMONY

12.11.11

at

JAKABARING PALEMBANG

 

 

THE END @ COPYRIGHR DR IWAN SUWANDY 2011

The MS Disease Info(Penyakit Pelawak Pepeng)

 

MUSEUM DUNIA MAYA DR IWAN S.

Dr IWAN ‘S CYBERMUSEUM

 THE FIRST INDONESIAN CYBERMUSEUM

  MUSEUM DUNIA MAYA PERTAMA DI INDONESIA

   DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI

     PENDIRI DAN PENEMU IDE

      THE FOUNDER

    Dr IWAN SUWANDY, MHA

                     

The Driwan’s  Cybermuseum

special for Mas Pepeng.family and his friend in order to open the diesease mystery

Khusu buat Mas pepeng,family and teman-temannya serta para pengemarnya untuk mengungkap misteri penyakit yang dideritanya

Saya salut atas semangat Mas pepeng yang tetap kreatif walaupun menderita penyakit MS

Multiple sclerosis

 
 
 
Multiple sclerosis
Classification and external resources

Demyelination by MS. The CD68 colored tissue shows several macrophages in the area of the lesion. Original scale 1:100
ICD-10 G35
ICD-9 340
OMIM 126200
DiseasesDB 8412
MedlinePlus 000737
eMedicine neuro/228 oph/179 emerg/321 pmr/82 radio/461
MeSH D009103
GeneReviews Multiple Sclerosis Overview

Multiple sclerosis (abbreviated MS, known as disseminated sclerosis or encephalomyelitis disseminata) is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms.[1] Disease onset usually occurs in young adults, and it is more common in women.[1] It has a prevalence that ranges between 2 and 150 per 100,000.[2] MS was first described in 1868 by Jean-Martin Charcot.[3]

MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are contained within an insulating substance called myelin. In MS, the body’s own immune system attacks and damages the myelin. When myelin is lost, the axons can no longer effectively conduct signals.[4] The name multiple sclerosis refers to scars (scleroses—better known as plaques or lesions) particularly in the white matter of the brain and spinal cord, which is mainly composed of myelin.[3] Although much is known about the mechanisms involved in the disease process, the cause remains unknown. Theories include genetics or infections. Different environmental risk factors have also been found.[4][5]

Almost any neurological symptom can appear with the disease, and often progresses to physical and cognitive disability.[4] MS takes several forms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms).[6] Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as the disease advances.[6]

There is no known cure for multiple sclerosis. Treatments attempt to return function after an attack, prevent new attacks, and prevent disability.[4] MS medications can have adverse effects or be poorly tolerated, and many patients pursue alternative treatments, despite the lack of supporting scientific study. The prognosis is difficult to predict; it depends on the subtype of the disease, the individual patient’s disease characteristics, the initial symptoms and the degree of disability the person experiences as time advances.[7] Life expectancy of people with MS is 5 to 10 years lower than that of the unaffected population.[1]

indonesia version

Multiple sclerosis (disingkat MS, yang dikenal sebagai disebarluaskan sclerosis atau encephalomyelitis disseminata) adalah penyakit inflamasi di mana selubung mielin di sekitar akson lemak otak dan sumsum tulang belakang yang rusak, menyebabkan demielinasi dan jaringan parut serta spektrum yang luas dari tanda-tanda dan gejala [1]. Onset penyakit biasanya terjadi pada dewasa muda, dan lebih umum pada perempuan. [1] Ia memiliki prevalensi yang berkisar antara 2 dan 150 per 100.000. [2] MS pertama kali dijelaskan pada 1868 oleh Jean-Martin Charcot [3].

MS mempengaruhi kemampuan sel-sel saraf di otak dan sumsum tulang belakang untuk berkomunikasi satu sama lain secara efektif. Sel saraf berkomunikasi dengan mengirimkan sinyal-sinyal listrik yang disebut potensial aksi turun serat panjang yang disebut akson, yang terkandung dalam zat isolator yang disebut mielin. Pada MS, serangan tubuh sendiri sistem kekebalan tubuh dan kerusakan myelin. Ketika myelin hilang, akson tidak bisa lagi efektif melakukan sinyal. [4] nama multiple sclerosis mengacu pada bekas luka (scleroses-lebih dikenal sebagai plak atau lesi) khususnya dalam masalah putih otak dan sumsum tulang belakang, yang terutama terdiri mielin [3]. Meskipun banyak yang diketahui tentang mekanisme yang terlibat dalam proses penyakit, penyebabnya masih belum diketahui. Teori termasuk genetika atau infeksi. Berbagai faktor risiko lingkungan juga telah ditemukan [4] [5].

Hampir semua gejala neurologis dapat muncul dengan penyakit ini, dan sering berkembang menjadi cacat fisik dan kognitif [4]. MS mengambil beberapa bentuk, dengan gejala baru yang terjadi baik dalam serangan diskrit (kambuh bentuk) atau perlahan-lahan terakumulasi dari waktu ke waktu (bentuk progresif). [ 6] Antara serangan, gejala bisa hilang sepenuhnya, tapi masalah neurologis permanen sering terjadi, terutama karena kemajuan penyakit. [6]

Tidak ada obat dikenal untuk multiple sclerosis. Perawatan upaya untuk kembali berfungsi setelah serangan, mencegah serangan baru, dan mencegah kecacatan [4] MS obat dapat memiliki efek samping atau buruk ditoleransi, dan banyak pasien mengejar pengobatan alternatif,. Meskipun kurangnya mendukung studi ilmiah. Prognosis sulit untuk memprediksi;. Itu tergantung pada subtipe penyakit, karakteristik penyakit pasien individu, gejala awal dan tingkat kecacatan orang mengalami seiring kemajuan zaman [7] Harapan hidup orang dengan MS adalah 5 sampai 10 tahun lebih rendah dari populasi tidak terpengaruh [1].

Contents

 

Classification

Progression of MS subtypes

Several subtypes, or patterns of progression, have been described. Subtypes use the past course of the disease in an attempt to predict the future course. They are important not only for prognosis but also for therapeutic decisions. In 1996 the United States National Multiple Sclerosis Society standardized four subtype definitions:[6]

  1. relapsing remitting,
  2. secondary progressive,
  3. primary progressive, and
  4. progressive relapsing.

The relapsing-remitting subtype is characterized by unpredictable relapses followed by periods of months to years of relative quiet (remission) with no new signs of disease activity. Deficits suffered during attacks may either resolve or leave sequelae, the latter being more common as a function of time.[1] This describes the initial course of 80% of individuals with MS.[1] When deficits always resolve between attacks, this is sometimes referred to as benign MS,[8] although patients will still accrue some degree of disability in the long term.[1] The relapsing-remitting subtype usually begins with a clinically isolated syndrome (CIS). In CIS, a patient has an attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis.[1][9] However only 30 to 70% of persons experiencing CIS later develop MS..

indonesia version

Perkembangan subtipe MS

Beberapa subtipe, atau pola perkembangan, telah dijelaskan. Subtipe menggunakan saja masa lalu penyakit dalam upaya untuk memprediksi masa depan saja. Mereka penting tidak hanya untuk prognosis tetapi juga untuk keputusan terapeutik. Pada tahun 1996 Amerika Serikat National Multiple Sclerosis Masyarakat standar empat subtipe definisi: [6]

timbul kambuh,
sekunder progresif,
primer progresif, dan
kambuh progresif.
Subtipe hilang-timbul kambuh ditandai dengan tidak terduga diikuti oleh periode bulan untuk tahun relatif tenang (remisi) dengan tidak ada tanda-tanda aktivitas penyakit baru. Defisit menderita selama serangan baik dapat mengatasi atau meninggalkan gejala sisa, yang terakhir menjadi lebih umum sebagai fungsi waktu [1]. Ini menjelaskan program awal 80% dari individu dengan MS. [1] Ketika defisit selalu menyelesaikan antara serangan, ini kadang-kadang disebut sebagai MS jinak, [8] walaupun pasien masih akan bertambah beberapa derajat kecacatan dalam jangka panjang [1]. subtipe hilang-timbul biasanya dimulai dengan suatu sindrom klinis terisolasi (CIS). Dalam CIS, pasien memiliki serangan sugestif dari demielinasi, tetapi tidak memenuhi kriteria untuk multiple sclerosis. [1] [9] Namun hanya 30 sampai 70% dari orang mengalami CIS kemudian mengembangkan MS

 
 
 
 

Nerve axon with myelin sheath

Secondary progressive MS

Secondary progressive MS (sometimes called “galloping MS”) describes around 65% of those with an initial relapsing-remitting MS, who then begin to have progressive neurologic decline between acute attacks without any definite periods of remission.[1][6] Occasional relapses and minor remissions may appear.[6] The median time between disease onset and conversion from relapsing-remitting to secondary progressive MS is 19 years.[10] The primary progressive subtype describes the approximately 10–15% of individuals who never have remission after their initial MS symptoms.[11] It is characterized by progression of disability from onset, with no, or only occasional and minor, remissions and improvements.[6] The age of onset for the primary progressive subtype is later than for the relapsing-remitting, but similar to mean age of progression between the relapsing-remitting and the secondary progressive. In both cases it is around 40 years of age.[1]

Progressive relapsing MS describes those individuals who, from onset, have a steady neurologic decline but also suffer clear superimposed attacks. This is the least common of all subtypes.[6]

Atypical variants of MS with non-standard behavior have been described; these include Devic’s disease, Balo concentric sclerosis, Schilder’s diffuse sclerosis and Marburg multiple sclerosis. There is debate on whether they are MS variants or different diseases.[12] Multiple sclerosis also behaves differently in children, taking more time to reach the progressive stage.[1] Nevertheless they still reach it at a lower mean age than adults.[1]

indonesia version

Sekunder progresif MS

Sekunder progresif MS (kadang-kadang disebut “berderap MS”) menjelaskan sekitar 65% dari mereka dengan hilang-timbul MS awal, yang kemudian mulai memiliki penurunan neurologis progresif antara serangan akut tanpa periode tertentu remisi [1] [6]. Sesekali kambuh dan remisi kecil mungkin muncul [6] median waktu antara onset penyakit dan konversi dari hilang-timbul ke MS progresif sekunder adalah 19 tahun.. [10] subtipe progresif primer menjelaskan sekitar 10-15% individu yang tidak pernah memiliki pengampunan setelah gejala awal mereka MS [11]. Hal ini ditandai dengan perkembangan cacat dari awal, tanpa, atau hanya sesekali dan ringan, remisi dan perbaikan. [6] usia onset untuk subtipe progresif primer ini kemudian dibandingkan untuk kambuh -timbul, tetapi mirip dengan usia rata-rata perkembangan antara hilang-timbul dan progresif sekunder. Dalam kedua kasus itu adalah sekitar 40 tahun. [1]

MS kambuh Progresif menggambarkan orang-orang yang, dari awal, mengalami penurunan neurologis stabil tapi juga menderita serangan ditumpangkan jelas. Ini adalah yang paling umum dari semua subtipe. [6]

Atipikal varian dari MS dengan non-standar perilaku telah dijelaskan, ini termasuk penyakit Devic itu, Balo konsentris sclerosis, sklerosis menyebar Schilder dan sclerosis multiple Marburg. Ada perdebatan tentang apakah mereka MS varian atau penyakit yang berbeda [12] Multiple sclerosis juga berperilaku berbeda pada anak-anak, mengambil lebih banyak waktu untuk mencapai tahap progresif.. [1] Meskipun demikian mereka masih mencapainya pada usia rata-rata lebih rendah daripada orang dewasa

Signs and symptoms

Main symptoms of multiple sclerosis

A person with MS can suffer almost any neurological symptom or sign, including changes in sensation such as loss of sensitivity or tingling, pricking or numbness (hypoesthesia and paresthesia), muscle weakness, clonus, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia); problems in speech (dysarthria) or swallowing (dysphagia), visual problems (nystagmus, optic neuritis including phosphenes,[13][14] or diplopia), fatigue, acute or chronic pain, and bladder and bowel difficulties.[1] Cognitive impairment of varying degrees and emotional symptoms of depression or unstable mood are also common.[1] Uhthoff’s phenomenon, an exacerbation of extant symptoms due to an exposure to higher than usual ambient temperatures, and Lhermitte’s sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS although not specific.[1] The main clinical measure of disability progression and symptom severity is the Expanded Disability Status Scale or EDSS.[15]

Symptoms of MS usually appear in episodic acute periods of worsening (called relapses, exacerbations, bouts, attacks, or “flare-ups”), in a gradually progressive deterioration of neurologic function, or in a combination of both.[6] Multiple sclerosis relapses are often unpredictable, occurring without warning and without obvious inciting factors with a rate rarely above one and a half per year.[1] Some attacks, however, are preceded by common triggers. Relapses occur more frequently during spring and summer.[16] Viral infections such as the common cold, influenza, or gastroenteritis increase the risk of relapse.[1] Stress may also trigger an attack.[17] Pregnancy affects the susceptibility to relapse, with a lower relapse rate at each trimester of gestation. During the first few months after delivery, however, the risk of relapse is increased.[1] Overall, pregnancy does not seem to influence long-term disability. Many potential triggers have been examined and found not to influence MS relapse rates. There is no evidence that vaccination and breast feeding,[1] physical trauma,[18] or Uhthoff’s phenomenon[16] are relapse triggers.

 Causes

Most likely MS occurs as a result of some combination of genetic, environmental and infectious factors,[1] and possibly other factors like vascular problems.[19] Epidemiological studies of MS have provided hints on possible causes for the disease. Theories try to combine the known data into plausible explanations, but none has proved definitive.

indonesian version

Gejala Utama multiple sclerosis

Seseorang dengan MS dapat mengalami gejala neurologis hampir semua atau tanda, termasuk perubahan sensasi seperti kehilangan sensitivitas atau kesemutan, menusuk atau mati rasa (hypoesthesia dan paresthesia), kelemahan otot, clonus, kejang otot, atau kesulitan dalam bergerak; kesulitan dengan koordinasi dan keseimbangan (ataksia); masalah dalam pidato (disartria) atau menelan (disfagia), masalah visual (nystagmus, neuritis optik termasuk phosphenes, [13] [14] atau diplopia), nyeri kelelahan, akut atau kronis, dan kandung kemih dan usus kesulitan [1]. gangguan kognitif dari berbagai derajat dan gejala emosional dari depresi atau mood yang tidak stabil juga umum. [1] Uhthoff itu fenomena, eksaserbasi gejala yang masih ada karena eksposur lebih tinggi dari suhu lingkungan biasa, dan menandatangani Lhermitte, sebuah sensasi listrik yang berjalan di belakang ketika menekuk leher, terutama karakteristik dari MS meskipun tidak tertentu [1]. Ukuran klinis utama dari perkembangan dan keparahan gejala kecacatan adalah Skala Cacat Status Expanded atau EDSS. [15]

Gejala biasanya muncul MS dalam periode akut episodik yang memburuk (disebut kambuh, eksaserbasi, pertarungan, serangan, atau “flare-up”), dalam penurunan secara bertahap progresif fungsi neurologis, atau kombinasi keduanya sclerosis [6]. Beberapa kambuh sering tidak terduga, terjadi tanpa peringatan dan tanpa faktor menghasut yang jelas dengan tingkat jarang di atas satu setengah per tahun [1]. Beberapa serangan, bagaimanapun, adalah didahului oleh pemicu umum. Relaps terjadi lebih sering selama musim semi dan musim panas [16]. Infeksi virus seperti pilek, influenza, atau gastroenteritis meningkatkan risiko kambuh [1] Stres juga dapat memicu serangan [17]. Kehamilan mempengaruhi kerentanan terhadap kambuh,. dengan tingkat kekambuhan lebih rendah pada setiap trimester kehamilan. Selama beberapa bulan pertama setelah melahirkan, bagaimanapun, risiko kekambuhan meningkat. [1] Secara keseluruhan, kehamilan tampaknya tidak mempengaruhi kecacatan jangka panjang. Memicu banyak potensi telah diperiksa dan ditemukan tidak mempengaruhi tingkat MS kambuh. Tidak ada bukti bahwa vaksinasi dan menyusui, [1] trauma fisik, [18] atau fenomena Uhthoff itu [16] adalah pemicu kambuh.

 Penyebab
MS paling mungkin terjadi sebagai hasil dari beberapa kombinasi dari faktor genetik, lingkungan dan menular, [1] dan mungkin faktor-faktor lain seperti masalah vaskuler [19]. Studi epidemiologis dari MS telah memberikan petunjuk tentang kemungkinan penyebab penyakit. Teori mencoba untuk menggabungkan data yang dikenal dalam penjelasan yang masuk akal, tetapi tidak ada yang terbukti definitif

Genetics

HLA region of Chromosome 6. Changes in this area increase the probability of suffering MS.

MS is not considered a hereditary disease. However, a number of genetic variations have been shown to increase the risk of developing the disease.[20]

The risk of acquiring MS is higher in relatives of a person with the disease than in the general population, especially in the case of siblings, parents, and children.[4] The disease has an overall familial recurrence rate of 20%.[1] In the case of monozygotic twins, concordance occurs only in about 35% of cases, while it goes down to around 5% in the case of siblings and even lower in half-siblings. This indicates susceptibility is partly polygenically driven.[1][4]

It seems to be more common in some ethnic groups than others.[21]

Apart from familial studies, specific genes have been linked with MS. Differences in the human leukocyte antigen (HLA) system—a group of genes in chromosome 6 that serves as the major histocompatibility complex (MHC) in humans—increase the probability of suffering MS.[1] The most consistent finding is the association between multiple sclerosis and alleles of the MHC defined as DR15 and DQ6.[1] Other loci have shown a protective effect, such as HLA-C554 and HLA-DRB1*11.[1]

Environmental factors

Different environmental factors, both of infectious and non infectious origin have been proposed as risk factors for MS. Although some are partly modifiable, only further research—especially clinical trials—will reveal whether their elimination can help prevent MS.[22]

MS is more common in people who live farther from the equator, although many exceptions exist.[1] Decreased sunlight exposure has been linked with a higher risk of MS.[22] Decreased vitamin D production and intake has been the main biological mechanism used to explain the higher risk among those less exposed to sun.[22][23][24]

Severe stress may also be a risk factor although evidence is weak.[22] Smoking has also been shown to be an independent risk factor for developing MS.[23] Association with occupational exposures and toxins—mainly solvents—has been evaluated, but no clear conclusions have been reached.[22]Vaccinations were also considered as causal factors for the disease; however, most studies show no association between MS and vaccines.[22] Several other possible risk factors, such as diet[25] and hormone intake, have been investigated; however, evidence on their relation with the disease is “sparse and unpersuasive”.[23]

Gout occurs less than would statistically be expected in people with MS, and low levels of uric acid have been found in MS patients as compared to normal individuals. This led to the theory that uric acid protects against MS, although its exact importance remains unknown.[26]

 Infections

Many microbes have been proposed as potential infectious triggers of MS, but none have been substantiated.[4]

Genetic susceptibility can explain some of the geographic and epidemiological variations in MS incidence, like the high incidence of the disease among some families or the risk decline with genetic distance, but does not account for other phenomena, such as the changes in risk that occur with migration at an early age.[5] An explanation for this epidemiological finding could be that some kind of infection, produced by a widespread microbe rather than a rare pathogen, is the origin of the disease.[5] Different hypotheses have elaborated on the mechanism by which this may occur. The hygiene hypothesis proposes that exposure to several infectious agents early in life is protective against MS, the disease being a response to a later encounter with such agents.[1] The prevalence hypothesis proposes that the disease is due to a pathogen more common in regions of high MS prevalence. This pathogen is very common, causing in most individuals an asymptomatic persistent infection. Only in a few cases, and after many years since the original infection, does it cause demyelination.[5][27] The hygiene hypothesis has received more support than the prevalence hypothesis.[5]

Evidence for viruses as a cause includes the presence of oligoclonal bands in the brain and cerebrospinal fluid of most patients, the association of several viruses with human demyelination encephalomyelitis, and induction of demyelination in animals through viral infection.[28] Human herpes viruses are a candidate group of viruses linked to MS. Individuals who have never been infected by the Epstein-Barr virus have a reduced risk of having the disease, and those infected as young adults have a greater risk than those who had it at a younger age.[1][5] Although some consider that this goes against the hygiene hypothesis, since the non-infected have probably experienced a more hygienic upbringing,[5] others believe that there is no contradiction since it is a first encounter at a later moment with the causative virus that is the trigger for the disease.[1] Other diseases that have also been related with MS are measles, mumps and rubella.[1]

Pathophysiology

 Blood-brain barrier breakdown

Demyelination in MS. On Klüver-Barrera myelin staining, decoloration in the area of the lesion can be appreciated (Original scale 1:100).

The blood–brain barrier is a capillary system that should prevent entrance of T cells into the nervous system.[4] The blood–brain barrier is normally not permeable to these types of cells, unless triggered by infection or a virus, which decreases the integrity of the tight junctions forming the barrier.[4] When the blood–brain barrier regains its integrity, usually after infection or virus has cleared, the T cells are trapped inside the brain.[4]

Autoimmunology

MS is currently believed to be an immune-mediated disorder mediated by a complex interaction of the individual’s genetics and as yet unidentified environmental insults.[4] Damage is believed to be caused by the patient’s own immune system. The immune system attacks the nervous system, possibly as a result of exposure to a molecule with a similar structure to one of its own.[4]

Lesions

The name multiple sclerosis refers to the scars (scleroses – better known as plaques or lesions) that form in the nervous system. MS lesions most commonly involve white matter areas close to the ventricles of the cerebellum, brain stem, basal ganglia and spinal cord; and the optic nerve. The function of white matter cells is to carry signals between grey matter areas, where the processing is done, and the rest of the body. The peripheral nervous system is rarely involved.[4]

More specifically, MS destroys oligodendrocytes, the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals.[4] MS results in a thinning or complete loss of myelin and, as the disease advances, the cutting (transection) of the neuron’s extensions or axons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.[4] A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes cannot completely rebuild the cell’s myelin sheath.[29] Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons.[29] Different lesion patterns have been described.[30]

Inflammation

Apart from demyelination, the other pathologic hallmark of the disease is inflammation. According to a strictly immunological explanation of MS, the inflammatory process is caused by T cells, a kind of lymphocyte. Lymphocytes are cells that play an important role in the body’s defenses.[4] In MS, T cells gain entry into the brain via the previously described blood–brain barrier. Evidence from animal models also point to a role of B cells in addition to T cells in development of the disease.[31]

The T cells recognize myelin as foreign and attack it as if it were an invading virus. This triggers inflammatory processes, stimulating other immune cells and soluble factors like cytokines and antibodies. Leaks form in the blood–brain barrier, which in turn cause a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins.[4]

Diagnosis

T1-weighted MRI scans (post-contrast) of the same brain slice at monthly intervals. Bright spots indicate active lesions.

Multiple sclerosis can be difficult to diagnose since its signs and symptoms may be similar to other medical problems.[1][32] Medical organizations have created diagnostic criteria to ease and standardize the diagnostic process especially in the first stages of the disease.[1] Historically, the Schumacher and Poser criteria were both popular.[33]

Currently, the McDonald criteria focus on a demonstration with clinical, laboratory and radiologic data of the dissemination of MS lesions in time and space for non-invasive MS diagnosis, though some have stated that the only proved diagnosis of MS is autopsy, or occasionally biopsy, where lesions typical of MS can be detected through histopathological techniques.[1][34][35]

Clinical data alone may be sufficient for a diagnosis of MS if an individual has suffered separate episodes of neurologic symptoms characteristic of MS.[34] Since some people seek medical attention after only one attack, other testing may hasten and ease the diagnosis. The most commonly used diagnostic tools are neuroimaging, analysis of cerebrospinal fluid and evoked potentials. Magnetic resonance imaging of the brain and spine shows areas of demyelination (lesions or plaques). Gadolinium can be administered intravenously as a contrast to highlight active plaques and, by elimination, demonstrate the existence of historical lesions not associated with symptoms at the moment of the evaluation.[34][36] Testing of cerebrospinal fluid obtained from a lumbar puncture can provide evidence of chronic inflammation of the central nervous system. The cerebrospinal fluid is tested for oligoclonal bands of IgG on electrophoresis, which are inflammation markers found in 75–85% of people with MS.[34][37] The nervous system of a person with MS responds less actively to stimulation of the optic nerve and sensory nerves due to demyelination of such pathways. These brain responses can be examined using visual and sensory evoked potentials.[38]

Management

Although there is no known cure for multiple sclerosis, several therapies have proven helpful. The primary aims of therapy are returning function after an attack, preventing new attacks, and preventing disability. As with any medical treatment, medications used in the management of MS have several adverse effects. Alternative treatments are pursued by some patients, despite the shortage of supporting, comparable, replicated scientific study.

Acute attacks

During symptomatic attacks, administration of high doses of intravenous corticosteroids, such as methylprednisolone, is the routine therapy for acute relapses.[1] Although generally effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on long-term recovery.[39] Oral and intravenous administration seem to have similar efficacy.[40] Consequences of severe attacks which do not respond to corticosteroids might be treated by plasmapheresis.[1]

Disease-modifying treatments

Disease-modifying treatments are expensive and most of these require frequent (up-to-daily) injections. Others require IV infusions at 1–3 month intervals.

Fingolimod (trade name Gilenya) was approved for MS by the FDA in 2010, and in Europe in 2011. As of 2011[update], after this approval, there are six disease-modifying treatments for MS approved by regulatory agencies of various countries, being the other five: Interferon beta-1a (trade names Avonex, CinnoVex, ReciGen and Rebif) and interferon beta-1b (U.S. trade name Betaseron, in Europe and Japan Betaferon). A third medication is glatiramer acetate (Copaxone), a non-interferon, non-steroidal immunomodulator. The fourth medication, mitoxantrone, is an immunosuppressant also used in cancer chemotherapy. The fifth is a humanized monoclonal antibody immunomodualtor, natalizumab (marketed as Tysabri).[1] The interferons and glatiramer acetate are delivered by frequent injections, varying from once-per-day for glatiramer acetate to once-per-week (but intra-muscular) for Avonex. Natalizumab and mitoxantrone are given by IV infusion at monthly intervals.

All six kinds of medications are modestly effective at decreasing the number of attacks in relapsing-remitting MS (RRMS) while the capacity of interferons and glatiramer acetate is more controversial. Studies of their long-term effects are still lacking.[1][41] Comparisons between immunomodulators (all but mitoxantrone) show that the most effective is natalizumab, both in terms of relapse rate reduction and halting disability progression.[42] Mitoxantrone may be the most effective of them all; however, it is generally not considered as a long-term therapy, as its use is limited by severe secondary effects.[1][41] The earliest clinical presentation of RRMS is the clinically isolated syndrome (CIS). Treatment with interferons during an initial attack can decrease the chance that a patient will develop clinical MS.[1]

Treatment of progressive MS is more difficult than relapsing-remitting MS. Mitoxantrone has shown positive effects in patients with secondary progressive and progressive relapsing courses. It is moderately effective in reducing the progression of the disease and the frequency of relapses in patients in short-term follow-up.[43] No treatment has been proven to modify the course of primary progressive MS.[44]

As with many medical treatments, these treatments have several adverse effects. One of the most common is irritation at the injection site for glatiramer acetate and the interferon treatments. Over time, a visible dent at the injection site, due to the local destruction of fat tissue, known as lipoatrophy, may develop. Interferons produce symptoms similar to influenza;[45] some patients taking glatiramer experience a post-injection reaction manifested by flushing, chest tightness, heart palpitations, breathlessness, and anxiety, which usually lasts less than thirty minutes.[46] More dangerous but much less common are liver damage from interferons,[47] severe cardiotoxicity, infertility, and acute myeloid leukemia of mitoxantrone,[1][41] and the putative link between natalizumab and some cases of progressive multifocal leukoencephalopathy.[1]

Management of the effects of MS

Disease-modifying treatments reduce the progression rate of the disease, but do not stop it. As multiple sclerosis progresses, the symptomatology tends to increase. The disease is associated with a variety of symptoms and functional deficits that result in a range of progressive impairments and disability. Management of these deficits is therefore very important. Both drug therapy and neurorehabilitation have shown to ease the burden of some symptoms, though neither influences disease progression.[1][48] Some symptoms have a good response to medication, such as unstable bladder and spasticity, while management of many others is much more complicated.[1] As for any patient with neurologic deficits, a multidisciplinary approach is key to improving quality of life; however, there are particular difficulties in specifying a ‘core team’ because people with MS may need help from almost any health profession or service at some point.[1] Multidisciplinary rehabilitation programs increase activity and participation of patients but do not influence impairment level.[49]

Historically, individuals suffering from MS were advised against participation in physical activity due to worsening symptoms.[50] However, under the direction of a physiotherapist, participation in physical activity can be safe and has been proven beneficial for patients with MS.[51] Research has supported the rehabilitative role of physical activity in improving muscle power,[52] mobility,[52] mood,[53] bowel health,[54] general conditioning and quality of life.[52] However, it is important to be cautious about not overworking or overheating the patient during the course of exercise. Physiotherapists have the expertise needed to adequately prescribe exercise programs that are suitable for the individual. The FITT equation (frequency of exercise, intensity of exercise, type of exercise and time/duration of exercise) is typically used to prescribe exercises.[51] Depending on the patient, activities may include resistance training,[55] walking, swimming, yoga, tai chi, and others.[54] Determining an appropriate and safe exercise program is challenging and must be carefully individualized to each patient being sure to account for all contraindications and precautions.[51]

 Alternative treatments

As with most chronic diseases, alternative treatments for multiple sclerosis, which are unsupported by clinical or scientific evidence, are pursued by some patients.[56] Examples are a dietary regimen,[57] herbal medicine (including the use of medical cannabis),[58] hyperbaric oxygenation[59] and self-infection with hookworm (known generally as helminthic therapy).[60]

 Prognosis

Disability-adjusted life yearfor multiple sclerosis per 100,000 inhabitants in 2004

  no data
  less than 13
  13–16
  16–19
  19–22
  22–25
  25–28
  28–31
  31–34
  34–37
  37–40
  40–43
  more than 43

The prognosis (the expected future course of the disease) for a person with multiple sclerosis depends on the subtype of the disease; the individual’s sex, age, and initial symptoms; and the degree of disability the person experiences.[7] The disease evolves and advances over decades, 30 being the mean years to death since onset.[1]

Female sex, relapsing-remitting subtype, optic neuritis or sensory symptoms at onset, few attacks in the initial years and especially early age at onset, are associated with a better course.[7][61]

The life expectancy of people with MS is 5 to 10 years lower than that of unaffected people.[1] Almost 40% of patients reach the seventh decade of life.[61] Nevertheless, two-thirds of the deaths in people with MS are directly related to the consequences of the disease.[1] Suicide also has a higher prevalence than in the healthy population, while infections and complications are especially hazardous for the more disabled ones.[1]

Although most patients lose the ability to walk prior to death, 90% are still capable of independent walking at 10 years from onset, and 75% at 15 years.[61][62]

Epidemiology

Ethnic groups such as the Sami have a lower incidence of MS, possibly due to genetic factors.

Two main measures are used in epidemiological studies: incidence and prevalence. Incidence is the number of new cases per unit of person–time at risk (usually number of new cases per thousand person–years); while prevalence is the total number of cases of the disease in the population at a given time. Prevalence is known to depend not only on incidence, but also on survival rate and migrations of affected people. MS has a prevalence that ranges between 2 and 150 per 100,000 depending on the country or specific population.[2] Studies on populational and geographical patterns of epidemiological measures have been very common in MS,[27] and have led to the proposal of different etiological (causal) theories.[5][22][23][27]

MS usually appears in adults in their thirties but it can also appear in children.[1] The primary progressive subtype is more common in people in their fifties.[11] As with many autoimmune disorders, the disease is more common in women, and the trend may be increasing.[1][63] In children, the sex ratio difference is higher,[1] while in people over fifty, MS affects males and females almost equally.[11]

There is a north-to-south gradient in the northern hemisphere and a south-to-north gradient in the southern hemisphere, with MS being much less common in people living near the equator.[1][63] Climate, sunlight and intake of vitamin D have been investigated as possible causes of the disease that could explain this latitude gradient.[23] However, there are important exceptions to the north–south pattern and changes in prevalence rates over time;[1] in general, this trend might be disappearing.[63] This indicates that other factors such as environment or genetics have to be taken into account to explain the origin of MS.[1] MS is also more common in regions with northern Europe populations.[1] But even in regions where MS is common, some ethnic groups are at low risk of developing the disease, including the Samis, Turkmen, Amerindians, Canadian Hutterites, Africans, and New Zealand Māori.[64]

Environmental factors during childhood may play an important role in the development of MS later in life. Several studies of migrants show that if migration occurs before the age of 15, the migrant acquires the new region’s susceptibility to MS. If migration takes place after age 15, the migrant retains the susceptibility of his home country.[1][22] However, the age–geographical risk for developing multiple sclerosis may span a larger timescale.[1] A relationship between season of birth and MS has also been found which lends support to an association with sunlight and vitamin D. For example fewer people with MS are born in November as compared to May.[65]

 History

Medical discovery

Detail of drawing from Carswell book depicting MS lesions in the brain stem and spinal cord (1838)

The French neurologist Jean-Martin Charcot (1825–1893) was the first person to recognize multiple sclerosis as a distinct disease in 1868.[66] Summarizing previous reports and adding his own clinical and pathological observations, Charcot called the disease sclerose en plaques. The three signs of MS now known as Charcot’s triad 1 are nystagmus, intention tremor, and telegraphic speech, though these are not unique to MS. Charcot also observed cognition changes, describing his patients as having a “marked enfeeblement of the memory” and “conceptions that formed slowly”.[3]

Prior to Charcot, Robert Carswell (1793–1857), a British professor of pathology, and Jean Cruveilhier (1791–1873), a French professor of pathologic anatomy, had described and illustrated many of the disease’s clinical details, but did not identify it as a separate disease.[66] Specifically, Carswell described the injuries he found as “a remarkable lesion of the spinal cord accompanied with atrophy”.[1] Under the microscope, Swiss pathologist Georg Eduard Rindfleisch (1836–1908) noted in 1863 that the inflammation-associated lesions were distributed around blood vessels.[67][68]

After Charcot’s description, Eugène Devic (1858–1930), Jozsef Balo (1895–1979), Paul Ferdinand Schilder (1886–1940), and Otto Marburg (1874–1948) described special cases of the disease. During all the 20th century there was an important development on the theories about the cause and pathogenesis of MS while efficacious treatments began to appear in 1990.[1]

 Historical cases

There are several historical accounts of people who lived before or shortly after the disease was described by Charcot and probably had MS.

1.Halidora

A young woman called Halldora, who lived in iceland around 1200, suddenly lost her vision and mobility, but after praying to the saints, recovered them seven days after.

Saint Lidwina of Schiedam (1380–1433),

 a Dutch nun, may be one of the first clearly identifiable MS patients. From the age of 16 until her death at 53, she suffered intermittent pain, weakness of the legs, and vision loss—symptoms typical of MS.[69] Both cases have led to the proposal of a ‘Viking gene’ hypothesis for the dissemination of the disease.[70]

3.Augustus Frederick d’Este (1794–1848),

son of Prince Augustus Frederick, Duke of Sussex and Lady Augusta Murray and the grandson of George III of the United Kingdom, almost certainly suffered from MS. D’Este left a detailed diary describing his 22 years living with the disease. His diary began in 1822 and ended in 1846, although it remained unknown until 1948. His symptoms began at age 28 with a sudden transient visual loss (amaurosis fugax) after the funeral of a friend. During the course of his disease, he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbances, and erectile dysfunction. In 1844, he began to use a wheelchair. Despite his illness, he kept an optimistic view of life.[71][72]

4.WNP Barbelion

Another early account of MS was kept by the British diarist W. N. P. Barbellion, nom-de-plume of Bruce Frederick Cummings (1889–1919), who maintained a detailed log of his diagnosis and struggle with MS.[72] His diary was published in 1919 as The Journal of a Disappointed Man.[73]

5.Indonesian Artist Pepeng

 

Stay in the Hospital Comforts Pepeng

- Ferrasta Soebardi alias Pepeng did not give up.
His passion to entertain, work, and science menutuntut never extinguished, although the disease Multiple gnawing Scleorosis since March 2005.
The house is located dipertemuan Pepeng two watershed, precisely at the very back corner of the Earth Heritage Complex Cinere, Depok, a lot changed. Not only that, his hobby of hanging out in pengkolan also never again dilakoninya. Now dive into the life he learned from the bed where he lay suffering from the disease. “Many consider me sick because of the location of this house. I do not believe it. I am more afraid of thieves than a ghost, “joke.
The proof, every day something came to my house Pepeng. Not to put a sense of pity, but instead draw from the life sciences Pepeng.
It has been over five years Pepeng friends with Scleorosis Multiple disease (MS). Rare disease that makes the sufferer paralyzed. Even at a specific stage of the autonomic nervous taxable, the brain can go wrong command.
However, the disease which attacked him did not make Pepeng stop ‘ngebanyol’. Although the actions that had to do with his group, Sergeant Geronimo ‘, currently only done while lying in bed. Pepeng obstinacy, in addition to fighting the disease, also encouraged a love that never faded from his beloved wife, Siti Aishah Mariam Utami. “Love it makes my life as it is now,” said Pepeng when met recently.
Not just trying to make a living, in the midst of the struggle against diseases, remains persistent Pepeng studying to reach his goal earned a Bachelor Two (S2) in Post Graduate, Faculty of Psychology, University of Indonesia. Master’s degree in the field of Social Psychology Interventions achieved with the predicate ‘cum laude’ in 2006.
Not quite just that, Pepeng also berancana continuing education to a doctorate (S3). Pepeng spirit is once again showing and proving that the conditions of her condition at this time does not become an obstacle to academic achievement. “Hopefully I can reach S3,” said Pepeng vigorously.

Got a ‘wife’ New

Pepeng first glance seemed helpless because the condition can only lie in bed and wheelchair. However, the same conditions which made him even more excited to have a ‘wife’ new. Thus, his days are never quiet from a busy work ‘wife’ a new form of a laptop which he uses to develop his new business, sell the domain.
Even according to his wife, Utami, new activities Pepeng with his laptop had become like his own wife. “Wake up he immediately held a ‘wife’ new and can take hours. If I only ‘wife’ second. His new wife, yes the laptop, “explains Utami. With the same tool Pepeng working on a book about his life that was nearly completed, he added.
Indeed Pepeng illness, can no longer make a career in the performing and entertainment presenter. However, he would still be a man who is fortunate to have a pious wife. So Pepeng remains strong and able to meet the needs of families by performing a number of activities such as Moslem received stitches in his home.
In diseased condition, Pepeng also able to send their children to college broadcast in the neighbor country, Malaysia. “Honestly, almost Mamas education is hampered due to lack of fees. However, before the tuition payment deadline, some colleagues came to see her deliver the fees and others. With the money, eventually Mamas could continue his studies again. All this because God intervened, “he said.

Want Not Lost Meaning of Life

Pepeng also revealed exposures of MS disease-fighting spirit that attacked since last five years. “I can only pray and most importantly, the spirit should not be extinguished. I maker crowd. My prayer when the first pain is not to lonely because of my behavior. I know, all diseases are created at once with the medicine. Hopefully I still miss the cure, “jokes the father of Mamas, Mio, Lalo, and Izra it.
Once convicted of MS disease, Pepeng space is very limited. His days were spent more in the bedroom. From the bedroom, too, Pepeng work. Every Tuesday from morning until evening, Pepeng shooting for the show program ‘Meet Pepeng’ from her bedroom.
In the bedroom newly renovated it, Pepeng also receive his guests. He never refused to those who want to visit. An acquaintance of the Facebook social networking account, for example, comes with 100 colleagues sekantornya invites. There was absolutely no privacy in the home space Pepeng and he only comes once limited to 30 guests still have some breathing room in a room measuring 6 x 7 meters.
Madura typical joke has always been a fresh distraction while talking with the guests. However, every speech, Pepeng bombarded true pain. Because the jokes fresh and warm greeting, the other person often forget that Pepeng was ill. Pepeng actually able to spread the spirit of life and the laptop remains the flagship for a relationship with the outside world. O ato

BIODATA Pepeng
Birth name: Ferrasta Soebardi
Date of Birth: 23 September 1954)
Place of Birth: Sumenep, Madura, Indonesia
Wife: Siti Aishah Mariam Utami
Children: Mamas, Mio, Lalo, and Izra
Occupation: Presenter, actor, writer
Years active: 1978 – present
Education: Graduate School of Psychology, University of Indonesia, majoring in Psychology of Social Intervention, passed August 4, 2006 with a very satisfactory value (A).
Which movie Starring: Rojali and Juleha (1979), Win-Delicious (1986), and his goods You (1986).
Work Experience: Employee Bank Pinaesaan (1988) and Bakrie Brothers (1989)

 
 
Ferrasta “Pepeng” Soebardi: “I’m Just Waiting for God’s Promise”
Rarely found who are grateful when wracked exam. Ferrasta Soebardi or better known as Pepeng is the one who bit it. In the middle of exams in the form of chronic pain that he could still smile and prejudice either to God.

Pepeng bersama istri tercinta

As is known, since five years ago, convicted Pepeng rare disease Multiple Sclerosis (MS), which is a disease that attacks the central nervous system and bring the process of inflammation (inflammation) of the spine. This disease will interfere with the delivery of “messages” between the brain and other body parts.
 

MS disease who suffered a former presenter of this famous cause paralysis and every moment felt incredible pain from waist to toe. How sakitkah? “As diketok mallet finger. But pain is not the time diketok, but after diketok. Carried away, carried away, carried away, “said Pepeng.

Pepeng sure there is wisdom behind a disease that God gives. He did not want depression and dissolve by this ordeal. This he proved by staying productive activity, although lived in the bed.

Pepeng admitted it when he gets sick a lot. Earned a master psychologist, for example. Even more closely interwoven friendship and wide when he was sick. Pepeng house almost every day on Earth Heritage Cinere guests visited Depok West Java, whether known or not. Not infrequently, many guests are enlightened after visiting the house Pepeng.

Middle of last month, Ahmad Damanik, Dadang Kusmayadi, Ibn Intercession, Saiful Hamiwanto, and Surya Fachrizal of Sound Hidayatullah visit to the residence Pepeng. This visit is solely for the interview, but also in the framework of friendship.

In the rooms there are many patches of paper testimonials from the guests, told the magazine Pepeng share stories of perseverance to face the disease

original info

Dalam Sakit Pepeng Tetap Menghibur

- Ferrasta Soebardi alias Pepeng tak menyerah.
Semangatnya untuk menghibur, berkarya, dan menutuntut ilmu tak pernah padam, walau penyakit Multiple Scleorosis menggerogotinya sejak Maret 2005.Rumah Pepeng yang terletak dipertemuan dua aliran sungai, persisnya di pojok paling belakang Kompleks Bumi Pusaka Cinere, Depok, banyak berubah. Tidak hanya itu, hobinya nongkrong di pengkolan juga tak pernah lagi dilakoninya. Kini dia belajar menyelami kehidupan dari atas ranjang tempatnya terbaring sejak menderita penyakit. “Banyak yang menganggap saya sakit karena lokasi rumah ini. Saya nggak percaya. Saya lebih takut maling daripada hantu,” kelakarnya.
Buktinya, setiap hari selalu ada saja yang datang ke rumah Pepeng. Bukan untuk menaruh rasa iba, tapi justru menimba ilmu hidup dari Pepeng.
Sudah lebih lima tahun Pepeng berteman akrab dengan penyakit Multiple Scleorosis (MS). Penyakit langka itu membuat penderitanya lumpuh. Bahkan pada stadium tertentu syaraf otonom kena, otak bisa salah perintah.
Namun, penyakit yang menyerangnya tak membuat Pepeng berhenti ‘ngebanyol’. Meskipun aksi-aksi yang dulu dilakukannya bersama grupnya, Sersan Prambors’, saat ini hanya dilakukannya sambil berbaring di tempat tidur. Ketegaran Pepeng, selain untuk melawan penyakitnya, juga didorong cinta kasih yang tak pupus dari istri tercintanya, Utami Mariam Siti Aisyah. “Cinta itu membuat saya hidup seperti sekarang,” kata Pepeng saat ditemui baru-baru ini. 
Tidak hanya berusaha mencari nafkah, di tengah perjuangan melawan penyakit, Pepeng tetap gigih menuntut ilmu untuk mewujudkan cita-citanya meraih gelar Strata Dua (S2) di  Pasca Sarjana, Fakultas Psikologi, Universitas Indonesia. Gelar master  dibidang Psikologi Intervensi Sosial diraihnya dengan predikat ‘cumlaude’ pada 2006 silam.
Tidak cukup hanya itu, Pepeng juga berancana melanjutkan pendidikan hingga meraih gelar doktor (S3). Semangat Pepeng ini sekaligus menunjukkan dan membuktikan bahwa kondisi yang kondisi yang dialaminya saat ini tidak menjadi kendala untuk mengukir prestasi akademik. “Mudah-mudahan saya mampu meraih S3,” ungkap Pepeng penuh semangat.Punya ‘Istri’ BaruSepintas Pepeng tampak tak berdaya karena kondisinya yang hanya bisa terbaring di tempat tidur dan kursi roda. Namun, kondisi itu pula yang membuatnya semakin bersemangat hingga memiliki ‘istri’ baru. Sehingga, hari-harinya tak pernah sepi dari kesibukan mengerjakan ‘istri’ baru berupa laptop yang digunakannya untuk mengembangkannya bisnis barunya, menjual domain.
Bahkan menurut istrinya, Utami, kegiatan baru Pepeng bersama laptopnya sudah dijadikan layaknya istri sendiri. “Bangun tidur dia langsung megang ‘istri’ barunya dan bisa berjam-jam. Kalau saya cuma ‘istri’ kedua. Istri barunya, ya laptop,” jelas Utami. Dengan alat itu pula Pepeng menggarap buku tentang kehidupannya yang sudah hampir rampung, tambahnya.
Memang penyakit yang diderita Pepeng, membuatnya tak bisa lagi tampil berkarir di dunia presenter dan entertainment. Namun, dia tetap masih menjadi seorang pria yang beruntung karena memiliki istri yang soleh. Sehingga Pepeng tetap tegar dan mampu memenuhi kebutuhan keluarga dengan melakukan sejumlah  kegiatan seperti menerima jahitan busana muslim di rumahnya.
Dalam kondisi sakit, Pepeng juga mampu menyekolahkan anaknya kuliah broadcast di negeri Jiran, Malaysia. “Jujur saja, pendidikan Mamas nyaris terhambat karena ketiadaan biaya. Namun, sebelum batas waktu pembayaran kuliah, beberapa rekan datang menjenguk sambil mengantarkan honor dan lain-lainnya. Dengan uang itu, akhirnya Mamas bisa melanjutkan kuliahnya kembali. Semua ini karena turut campur tangan Allah,” ungkapnya.Tak Mau Kehilangan Makna HidupPepeng juga mengungkapkan, ikhwal semangatnya melawan penyakit MS yang menyerangnya sejak lima tahun terakhir. “Saya hanya bisa berdoa dan yang paling penting, semangat tidak boleh padam. Saya pembuat keramaian. Doa saya ketika pertama sakit adalah jangan sampai kesepian karena perilaku saya.  Saya tahu, semua penyakit diciptakan sekaligus dengan obatnya. Mudah-mudahan saya masih kebagian obatnya,” kelakar ayah dari Mamas, Mio, Lalo, dan Izra itu.
Setelah divonis penyakit MS, ruang gerak Pepeng memang sangat terbatas. Hari-harinya lebih banyak dihabiskan di kamar tidur. Dari kamar tidur itu pula, Pepeng bekerja. Tiap Selasa sejak pagi hingga petang, Pepeng melakukan pengambilan gambar untuk program acara ‘Ketemu Pepeng’ dari ruang tidurnya.
Di kamar tidur yang baru direnovasi itu, Pepeng juga menerima tamu-tamunya. Dia tak pernah menolak orang-orang yang ingin bertandang. Seorang kenalan dari akun jejaring sosial Facebook, misalnya, datang dengan mengajak 100 rekan sekantornya. Sama sekali tak ada ruang privasi di rumah Pepeng dan dia hanya membatasi 30 tamu sekali datang agar tetap punya ruang bernapas di kamar berukuran 6 x 7 meter itu.
Guyonan khas Madura selalu menjadi selingan segar ketika berbincang dengan para tamu. Tetapi, setiap berbicara, Pepeng sejatinya dihujani rasa sakit. Karena guyonan segar dan sapaan hangatnya, lawan bicara sering lupa bahwa Pepeng sedang sakit. Pepeng justru mampu menebar semangat hidup dan laptop tetap menjadi andalannya untuk menjalin hubungan dengan dunia luar. O atoBIODATA PEPENG
Nama lahir        : Ferrasta Soebardi
Tanggal Lahir    : 23 September 1954)
Tempat Lahir    : Sumenep, Madura, Indonesia
Istri                : Utami Mariam Siti Aisyah
Anak            : Mamas, Mio, Lalo, dan Izra
Pekerjaan         : Presenter, aktor, penulis
Tahun aktif         : 1978 – sekarang
Pendidikan        : Pasca Sarjana Fakultas Psikologi Universitas Indonesia, jurusan Psikologi Intervensi Sosial, lulus 4 Agustus 2006 dengan nilai sangat memuaskan (A).
Film Yang Dibintangi: Rojali dan Juleha (1979), Sama-Sama Enak (1986), dan Anunya Kamu (1986).
Pengalaman Kerja:  Pegawai Bank Pinaesaan (1988) dan Bakrie Brothers (1989)
 
 
 

Ferrasta “Pepeng” Soebardi:“Saya Tinggal Menunggu Janji Allah” 

Jarang sekali ditemukan orang yang bersyukur ketika didera ujian. Ferrasta Soebardi atau lebih dikenal dengan Pepeng adalah orang yang sedikit itu. Di tengah ujian berupa sakit yang menahun ia masih bisa tersenyum dan berprasangka baik kepada Allah.

Pepeng bersama istri tercinta 

Seperti diketahui,  sejak lima tahun silam, Pepeng divonis penyakit langka  Multiple Sclerosis (MS-red), yakni sebuah penyakit yang menyerang sistem saraf pusat dan memunculkan terjadinya proses inflamasi(peradangan) pada tulang belakang. Penyakit ini akan mengganggu penyampaian “pesan” antara otak dan bagian-bagian tubuh lainnya.

 

Penyakit MS yang dideritanya menyebabkan mantan presenter kondang ini mengalami kelumpuhan dan setiap saat merasakan nyeri yang luar biasa dari pinggang hingga ujung kaki. Seberapa sakitkah? “Seperti jari diketok palu. Tapi nyerinya bukan saat diketok, tapi setelah diketok. Nyut, nyut,nyut,” kata Pepeng.

Pepeng yakin ada hikmah di balik penyakit yang Allah berikan. Ia tak ingin depresi dan larut oleh penderitaan yang dialaminya ini. Ini ia buktikan dengan tetap melakukan aktivitas yang produktif, meski dijalani di atas tempat tidur.

Pepeng mengaku justru saat sakit ia mendapatkan banyak hal. Memperoleh gelar master psikolog, misalnya. Jalinan pertemanannya pun semakin erat dan luas saat ia sakit. Hampir setiap harinya rumah Pepeng di Bumi Pusaka Cinere Depok Jawa Barat dikunjungi tamu, baik yang dikenal maupun yang tidak. Tak jarang banyak tamu yang tercerahkan setelah berkunjung ke rumah Pepeng.

Pertengahan bulan lalu, Ahmad Damanik, Dadang Kusmayadi, Ibnu Syafaat, Saiful Hamiwanto, dan Surya Fachrizal dari Suara Hidayatullah berkunjung ke kediaman Pepeng. Kunjungan kali ini tidak semata-mata untuk wawancara, tapi juga dalam rangka silaturahim.

Di dalam kamarnya yang terdapat banyak tempelan kertas testimoni dari para tamu itu, kepada majalah ini Pepeng berbagi kisah tentang ketabahannya menghadapi penyakit.

Research directions

 

 Therapies

Chemical structure of alemtuzumab

Research directions on MS treatments include investigations of MS pathogenesis and heterogeneity; research of more effective, convenient, or tolerable new treatments for RRMS; creation of therapies for the progressive subtypes; neuroprotection strategies; and the search for effective symptomatic treatments.[74] A number of treatments that may curtail attacks or improve function are under investigation. Emerging agents for RRMS that have shown promise in phase 2 trials include alemtuzumab (trade name Campath), daclizumab (trade name Zenapax), rituximab, dirucotide, BHT-3009, cladribine, dimethyl fumarate, estriol, fingolimod, laquinimod, minocycline, statins, temsirolimus and teriflunomide.[74]

In 2010, an FDA committee recommended approving fingolimod for the treatment of MS attacks,[75] and on September 22, 2010, fingolimod (trade name Gilenya) became the first oral drug approved by the Food and Drug Administration to reduce relapses and delay disability progression in patients with relapsing forms of multiple sclerosis.[76] Clinical trials of fingolimod have demonstrated side effects in treated patients, including cardiovascular conditions, macular edema, infections, liver toxicity and malignancies.[77][78]

Much interest has been focused on the prospect of utilizing vitamin D analogs in the prevention and management of CIS and MS, especially given its possible role in the pathogenesis of the disease. While there is anecdotal evidence of benefit for low dose naltrexone,[79] only results from a pilot study in primary progressive MS have been published.[80]

Disease biomarkers

The variable clinical presentation of MS and the lack of diagnostic laboratory tests lead to delays in diagnosis and the impossibility of predicting diagnosis. New diagnostic methods are being investigated. These include work with anti-myelin antibodies, analysis of microarray gene expression and studies with serum and cerebrospinal fluid but none of them has yielded reliable positive results.[81]

Currently there are no clinically established laboratory investigations available that can predict prognosis. However, several promising approaches have been proposed. Investigations on the prediction of evolution have centered on monitoring disease activity. Disease activation biomarkers include interleukin-6, nitric oxide and nitric oxide synthase, osteopontin, and fetuin-A.[81] On the other hand since disease progression is the result of neurodegeneration the roles of proteins indicative of neuronal, axonal, and glial loss such as neurofilaments, tau and N-acetylaspartate are under investigation.[81]

A final investigative field is work with biomarkers that distinguish between medication responders and nonresponders.[81]

Chronic cerebrospinal venous insufficiency

In 2008, Italian vascular surgeon Paolo Zamboni reported research suggesting that MS involves a vascular disease process he referred to as chronic cerebrospinal venous insufficiency (CCSVI, CCVI), in which veins from the brain are constricted. He found CCSVI in the majority of MS patients, performed a surgical procedure to correct it and claimed that 73% of patients improved.[82] Concern has been raised with Zamboni’s research as it was neither blinded nor controlled[83] and further studies have had variable results.[84] This has raised serious objections to the hypothesis of CCSVI originating multiple sclerosis.[85] The neurology community currently recommends not to use the proposed treatment until its effectiveness is confirmed by controlled studies, the need for which has been recognized by the scientific bodies engaged in MS research

the end @ copyright Dr iwan suwandy 2011