Ukkie Saraf Lbm 3

2013

Ukkie- modul saraf lbm 3 (STROKE)

STEP 1

1. Lesi hiperdens intrasulci adalah bayangan yang dihasilkan oleh alat Ct Scan karena terdapat adanya lesi atau kebocoran vaskuler pada sulcus cerebri 2. Alloanamnesa adalah anamnesa yang di pantau terus menerus , dengan orang lain. 3. Lesi hipodens adalah gambaran yang dihasilkan oleh Ct Scan karena kebocoran vaskuler , gambaran lebih rendah karena ada kematian  jaringan STEP 2

Nyeri kepala hebat Gangguan kesadaran Muntah TD 170/100 Kekakuan pada leher Hiperdens intrasulci Hipodens intrasulci daerah globus temporal kanan Tidak ditemukan defisit neurologis fokal (tidak ada Kehilangan Kehilangan persarafan lokal)

Vaskularisasi 1. Autoregulasi sirkulasi serebral? 2. Anatomi vaskularisasi lobus temporalis?

@ s i m a n g b e w o k  – m a n g b e w o k . t k

Page 1

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Ukkie- modul saraf lbm 3 (STROKE)

SUMBER : ATLAS ANATOMI YOKOCHI

2013

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Ukkie- modul saraf lbm 3 (STROKE)

5. Patogenesis kebocoran vaskuler ? TIK 1. 2. 3. 4. 5. 6. 7.

Faktor peningkatan TIK ? Sirkulasi LCS ? Gejala klinis dan tanda TIK naik ? Pemeriksaan Pemeriksaan penunjang ? Penatalaksanaa ? Komplikasi TIK naik ? Prognosis ?

DD perdarahan dalam otak 1. 2. 3. 4. 5. 6.

Etiologi ? Macam – macam perdarahan otak ? Gejala dari macam macam DD ? Patogenesis ? Komplikasi ? Penegakan diagnosa ?

defisit neurologis fokal 1. Definisi ? 2. Penyebanya ? 3. Patogenesis ?

STEP 3 Vaskularisasi 1. Autoregulasi sirkulasi serebral? TD perifer meningkat  arteri otak vasodilatasi (kompensasi) Faktor yang mengatur autoregulasi : o2, glukosa Proses ? 2. Anatomi vaskularisasi lobus temporalis?

2013

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Ukkie- modul saraf lbm 3 (STROKE)

2013

a.carotis interna a.optalmiica , a,comunicans posterior . a.cerebri media , a.cerebri anterior a.v ertebralis  r.meningea , a.spinalis superior et posterior , a.poterior inferior cerebeli, a.medularis sirkulasi wilisi  ada a.basilaris --. A.pontines ,a.labirintis,a.superior ,a.labirintis,a.superior cerebeli , a.cerebri posterior dan a.inferior a.inferior anterior cerebelli 3. Penyebab gangguan vaskularisasi? -aterosklerosis vasa otak trombositosis, emboli,  menyumbat atau pecah Sumbatan ? Pecah ?

4. Macam macam gangguan vaskularisasi otak? Pada semua lobus (fungsi,vaskuler) (fungsi,vaskuler) 5. Patogenesis kebocoran vaskuler ? Sumbatan : sumbatan arteri otak  pecah  fagosit kerusakanfoam sel (makrofag)  arteri lainnya  iskemic  cairan plasma keluar  TIK naik  nyeri SNH Penyumbatan  vasodilatasi maximal  vaskuler kolateral  peningkatan tekananhidrostatik  cairan vaskuler kluar  TIK naik  hilangnya autoregulasi meningkat  kekakuan vaskuler ppada kondisi vasodilatasi  hipertensi  pecah SH TIK 1. Faktor peningkatan TIK ? LCS , vaskuler , masa 2. Sirkulasi LCS ? Plexus coroideus  ventrikel lateral tersisu ventrikel lewat foramen intraventrikularis monroi  ventrikel quartus lewat aqueductus

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Ukkie- modul saraf lbm 3 (STROKE)

2013

akan lwat sisi lateral hemisferium , pada bagian inferior  lewat antara mdeulla spinalis dan cauda equina vili arachnoidea di absorbsi 3. Gejala klinis dan tanda TIK naik ?

Nyeri kepala, muntah , papil edem 4. Pemeriksaan Pemeriksaan penunjang ? Ct scan , EEG , EMG 5. Penatalaksanaan ? Penderita DM  obat DM Hypertensi  obat anti hypertensi Perbaikan LS

6. Komplikasi TIK naik ? Hydrocefalus , stroke , allopesia ,gangguan pertumbuhan

7. Prognosis ? Prognosis buruk kalo tidak ditangani , tingkat keparahan tinggi DD perdarahan dalam otak 1. Etiologi ? Hydrocefalus Stroke hemoragic Perbedaan Stroke Hemoragic dan Stroke Non Hemoragic ?

2. 3. 4. 5.

Macam – macam perdarahan otak ? Faktor Resiko ? Gejala dari macam macam DD ? Patogenesis ?

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2013

Ukkie- modul saraf lbm 3 (STROKE)

defisit neurologis fokal 1. Definisi ? 2. Penyebanya ? 3. Patogenesis ? STROKE 1. Definisi Sindroma akibat lesi vaskuler ragional di batang otan . di sub kortikal atau di kortikal Pukulan mendadak 2. Macam macam stroke 3. Patogenesis 4. Faktor resiko stroke 5. Penegakan diagnosa

STEP 4 Autoregulasi

TD perifer meningkat

LCS turun

O2 , CO2 , glukosa Monosit makrofag PECAH

Faktor resiko Foam cell

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Ukkie- modul saraf lbm 3 (STROKE) STEP 7

Vaskularisasi 1. Autoregulasi sirkulasi serebral? 2. Anatomi vaskularisasi lobus temporalis?

VASKULARISASI OTAK

Darah mengalir ke otak melalui dua arteri karotis dan dua arteri vertebralis.

2013

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Ukkie- modul saraf lbm 3 (STROKE)



2013

Arteri serebri anterior memberikan vaskularisasi pada korteks frontalis,

 parietalis bagian tengah, korpus kalosum dan nukleus nukleus kaudatus. 

Arteri serebri media memberikan vaskularisasi pada korteks lobus frontalis,

 parietalis dan temporalis.

Sistem vertebral dibentuk oleh arteri vertebralis kanan dan kiri yang berpangkal di arteri subklavia, menuju dasar tengkorak melalui kanalis transversalis di kolumna vertebralis servikalis, masuk rongga kranium melalui foramen magnum, lalu mempercabangkan masing-masing sepasang arteri serebeli inferior. Pada batas medula oblongata dan pons, keduanya bersatu menjadi arteri basilaris dan setelah mengeluarkan 3 kelompok cabang arteri, pada tingkat mesensefalon, arteri basilaris berakhir sebagai sepasang cabang arteri serebri posterior. posterior.



Arteri vertebralis memberikan vaskularisasi pada batang otak dan medula

spinalis atas. 

Arteri basilaris memberikan vaskularisasi pada pons.



Arteri serebri posterior memberikan vaskularisasi pada lobus temporalis,

oksipitalis, sebagian kapsula interna, talamus, hipokampus, korpus genikulatum dan mamilaria, pleksus koroid dan batang otak bagian atas.

http://www.scribd.com/doc/37484430/VASKULARISASI-O http://www .scribd.com/doc/37484430/VASKULARISASI-OT TAK

3. Penyebab gangguan vaskularisasi? -aterosklerosis vasa otak trombositosis, emboli,  menyumbat atau pecah Sumbatan ?

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Ukkie- modul saraf lbm 3 (STROKE)

2013

•

Afasia bila gangguan terletak pada sisi dominan (hemispherium kiri).

•

Hemiparesis kontra lateral dan dapat disertai sindrom Horner pada sisi sumbatan, terjadi akibat insufisiensi aliran darah arteria serebri media.

b. A.Serebri anterior

•

Hemiparesis kontra lateral dengan kelumpuhan tungkai lebih menonjol.

•

Gangguan mental (demensia) bila lesi berada di lo bus frontalis.

•

Inkontinensia.

•

Kejang-kejang.

c.

A. serebri media

•

Bila sumbatan di pangkal arteri, terjadi hemiparesis yang sama, bila tidak di pangkal maka lengan lebih menonjol.

•

Hemihipestesia.

•

Gangguan fungsi luhur pada korteks hemisfer hemisfer dominan (kiri) yang terserang terserang antara lain afasia motorik/sensorik.

d. Kedua sisi

•

Timbul gejala pseudobulbar : Hemiplegia dupleks, Sukar menelan, Gangguan emosional, mudah menangis.

•

Saraf kranial dan inti-intinya dapat terlibat dan menimbulkan kelumpuhan jenis neuron motorik perifer disertai atrofi otot, fenomena ini disebut sindroma paralisis bulbar.

2. Gejala-gejala penyumbatan sistem vertebralis

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Ukkie- modul saraf lbm 3 (STROKE)

2013

c. A. Cerebri Posterior inferior 

Sindrom Wallenberg



Sindrom Horner sesisi dengan lesi.



Disfagia, apabila infark mengenai nukleus ambigus ipsilateral.



Nistagmus, jika terjadi infark pada nukleus vestibularis.



Hemihipestesia alterans.



Gangguan sensorik



Koordinasi



Gangguan kesadaran

http://www.scribd.com/doc/37484430/VASKULARISASI-O http://www .scribd.com/doc/37484430/VASKULARISASI-OT TAK

5. Patogenesis kebocoran vaskuler ? Sumbatan : sumbatan arteri otak  pecah  fagosit kerusakanfoam sel (makrofag)  arteri lainnya  iskemic  cairan plasma keluar  TIK naik  nyeri SNH Penyumbatan  vasodilatasi maximal  vaskuler kolateral  peningkatan tekananhidrostatik  cairan vaskuler kluar  TIK naik  hilangnya autoregulasi meningkat  kekakuan vaskuler ppada kondisi vasodilatasi  hipertensi  pecah SH TIK 8. Faktor peningkatan TIK ? LCS , vaskuler , masa

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Ukkie- modul saraf lbm 3 (STROKE)

2013

10.Gejala 10.Gejala klinis dan tanda TIK naik ?

Nyeri kepala, muntah , papil edem AUTOREGULASI DAN METABOLISME

Pada kondisi istirahat, dialirkan sekitar 750cc darah permenit (15-20% cardiac output). Parameter penting dalam memperhitungkan aliran darah otak yang dinamakan tekanan perfusi cerebral (CPP), yang idealnya menggambarkan perbedaan mean tekanan arterial (MAP) dikurangi tekanan intra kranial (ICP). Diperkirakan bahwa pada CPP antara 50 dan 130 mmHg hanya terdapat sedikit, bila ada, variasi dalam CBF total. Sirkulasi carotis (anterior) memperoleh mayoritas aliran darah dalam kecepatan kecepatan yang lebih tinggi (335 cc/menit melalui setiap carotis) sedangkan sirkulasi posterior (vertebrobasiler), memperoleh 75 cc/menit. Lebih  jauh lagi, juga terdapat perbedaan antara substansia substansia grisea yang merupakan  jaringan dengan aliran cepat (64 cc/ 100 g/ menit) dengan substansia substansia alba yang merupakan jaringan dengan dengan aliran pelan (15-20 cc/ 100 g/ g / menit). Aliran darah juga terkait dengan aktivitas elektroserebral. Karena mekanisme otak dalam meregulasi aliran darahnya masih tidak jelas, maka terdapat beberapa teori yang diajukan. Teori Miogenik

Teori ini menyatakan bahwa pembuluh darah dapat mengenali aliran dan menyesuaikan diri terhadapya. Menurut Baliss dalam 1902, apabila tekanan dalam pembuluh darah meningkat, maka pembuluh darah tersebut akan berkontraksi untuk meningkatkan tahanannya sehingga mengurangi aliran darah. Teori Neurogenik

Edvinsson dkk menjelaskan berbagai bahwa terdapat berbagai saraf pada pembuluh darah piamater, yang menjelaskan mengenai regulasi sentral. Kerusakan

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Ukkie- modul saraf lbm 3 (STROKE)

2013

dapat digunakan. Simpanan glikogen dalam otak normal tidak ada, sehingga  jaringan saraf tergantung tergantung pada aliran kontinyu kontinyu dari pembuluh darah otak. Metabolisme anaerob menghasilkan peningkatan cepat jumlah laktat yang menurunkan pH dan meningkatkan ketersediaan ion H+ lokal. Parameter yang digunakan untuk menentukan aktivitas metabolik dinamakan CMRO2, atau metabolisme lokal otak dari O2. Diasumsikan bahwa penggunaan O2 merefleksikan merefleksikan metabolisme glukosa lokal dan hal ini dikonfirmasi dengan penggunaan scanning positron emission tomography (PET). Efek dari variasi kondisi metabolik yang normal dan yang berubah yang mempengaruhi CMRO2 dan dapat diukur, dapat membantu memecahkan masalah seputar peran dari mekanisme sentral dan umpan balik neurogenik dalam mengontrol CBF, sehingga bermanfaat untuk panduan terapi di masa yang akan datang. Faktor Lokal yang Mempengaruhi Autoregulasi Kondisi lokal lain tampaknya juga berperan dalam autoregulasi. Faktor ini meliputi pO2, pCO2, konsentrasi H+ dan pH lokal serta suhu. Efek individual dari faktor-faktor ini dapat diidentifikasi dengan segera, namun interaksi diantara faktorfaktor tersebut masih tetap kompleks. Oksigen Oksigen tidak akan mempengaruhi CBF hingga pO2 turun sampai dibawah 50 mmHg dimana CBF akan meningkat dengan cepat. Ketika pO2 sebesar 30 mmHg, CBF menjadi dua kali lipatnya. Hal ini kemungkinan bervariasi sesuai hematokrit. Peningkatan pO2 menginduksi sedikit penurunan CBF, ketika subyek normal bernafas dengan oksigen 100 % maka CBF berkurang 10 hingga 13%. Oksigen hiperbarik diberikan pada 2 atm akan menurunkan CBF sebesar 22 % tanpa merubah konsumsi oksigen otak. Penurunan ini tetap terjadi bahkan bila terjadi

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Ukkie- modul saraf lbm 3 (STROKE)

2013

Hiperventilasi, dengan pCO2 yang menurun, akan bermanfaat. Sayangnya, Sayangnya, saat SSP cepat menyesuaikan diri terhada perubahan ini, sukar untuk mengetahui berapa lama reaksi ini bertahan. Bahkan tampaknya pembuluh darah serebral juga menyesuaikan diri dalam 24 -36 jam. Hiperventilasi yang berkepanjangan memiliki efek yang buruk dengan menyebabkan menyebabkan iskemia. Peneliti yang lain memperoleh data dari manipulasi pCO2 secara langsung terhadap perubahan MAP dimana CBF akan bervariasi secara langsung dengan MAP pada area yang rusak dan tidak dipengaruhi oleh pCO2. Banyak ilmuwan yang berkonsentrasi dalam meneliti fenomena ”steal and countersteal” yang secara teoritis mungkin terjadi. Peneliti -peneliti tersebut mengajukan teori bahwa jika suatu bagian dari sirkulasi otak kehilangan kemampuan autoregulasinya, dan jika aliran yang melalui bagian tersebut berhubungan secara langsung dengan MABP, maka ketika Kalsium Saat ini peran ion Ca++ pada metabolisme dan aliran darah otak sedang diteliti secara intensif. Bukti-bukti yang mendukung mengenai peran aktif Ca++ dalam CBF mencakup peran Ca++ pada kontraksi otot dan peningkatan penggunaan Ca++ channel blocker dalam pengelolaan hipertensi dan penyakit arteri koroner. Lebih jauh lagi, influks dari Ca++ dianggap sebagai .. Konsentrasi ion Ca++ ekstraseluler ekstraseluler adalah sekitar 4-5 mEq/L dan konsentrasi konsentrasi Ca++ intraseluler adalah 107 mEq/L. PENGUKURAN ALIRAN DARAH OTAK Pertanyaan yang paling penting adalah bagaimana menetukan aliran darah sesungguhnya ke suatu bagian tertentu dari otak. Adolfo Fick menyatakan bahwa

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Ukkie- modul saraf lbm 3 (STROKE)

2013

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Ukkie- modul saraf lbm 3 (STROKE)

13.Komplikasi 13.Komplikasi TIK naik ? Hydrocefalus , stroke , allopesia ,gangguan pertumbuhan

14.Prognosis 14.Prognosis ? Prognosis buruk kalo tidak ditangani , tingkat keparahan tinggi DD perdarahan dalam otak 8. Etiologi ? Hydrocefalus Stroke hemoragic Perbedaan Stroke Hemoragic dan Stroke Non Hemoragic ?

9. Macam – macam perdarahan otak ? 10.Faktor 10.Faktor Resiko ? 11.Gejala 11.Gejala dari macam macam DD ? 12.Patogenesis 12.Patogenesis ? 13.Komplikasi 13.Komplikasi ?

2013

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2013

Ukkie- modul saraf lbm 3 (STROKE)

4. Definisi ? 5. Penyebanya ? Penyebab stroke Stroke banyak terjadi pada kelompok usia lanjut. Sama halnya dengan jantung koroner, pembuluh darah otak semakin hari semakin menebal. Diperlukan waktu puluhan

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Ukkie- modul saraf lbm 3 (STROKE)

2013

Penyebab seperti thrombus, embolus, cacing, parasit, atau leukemia yang dapat menyumbat pembuluh darah. 

Pecahnya pembuluh darah otak Pecahnya pembuluh darah otak dapat terjadi di ruang subarachnoid (di bawah

selaput otak) atau intracerebral (dalam jaringan otak). Akibatnya adalah darah dari arteri otak akan terus mengalir keluar tanpa ada yang dapat menghentikan. Darah akan menutupi dan menekan sebagian besar jaringan otak sehingga jaringan otak yang tertekan akan mengalami hipoksia disertai dengan kematian jaringan otak, bahkan mungkin disertai dengan kematian biologis. B. Faktor dari luar pembuluh darah 

Penurunan perfusi (aliran) darah ke otak Hal ini dapat disebabkan oleh berbagai hal seperti hipertensi menahun yang

menyebabkan terjadinya perubahan anatomi jantung, gagal jantung kongestif atau hiperkolesterol. Adanya perubahan tersebut menyebabkan darah menjadi relatif lebih pekat

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2013

Ukkie- modul saraf lbm 3 (STROKE)

 jangan sampai terjadi seranagn TIA ataupun stroke yang berulang. Pencegahan sekunder  dapat dilakukan dengan cara sebagai berikut: Stroke Council of the American Heart Association merekomendasikan hal pencegahan sebgai berikut :

Lemak

LDL < 100 mg/dL HDL > 35 mg/dL TC < 200 mg/dL TG < 200 mg/dL

 Alkohol

Mengurangi konsumsi alkohol

 Aktifitas fisik

30 –60 menit dalam 3-4 kali / menggu ≤ 120 % dari berat badan ideal

Diet AHA step II: ≤ 30 % l emak, < 7 % lemak jenuh, < 200 mg/hari kolesterol, penurunan berat badan dan aktifitas fisik. Jika target tak tercapai dan LDL > 130 mg/dL berikan terapi medikamentosa (mis: statin). Bila LDL 100-130 mg/dL, medikamentosa dapat dipertimbangkan. Edukasi pasien dan keluarga untuk kurangi / hentikan kebiasaan minum alcohol Latihan fisik sedang (jalan santai, jogging, bersepeda atau aerobik). Program dengan supersi medis bagi pasien dengan rsiko tinggi (penyakit jantung)

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Ukkie- modul saraf lbm 3 (STROKE)



2013

Kandungan lain yang berguna bagi pasien pasca stroke adalah fucoidan yaitu suatu polisakarida kompleks yang membantu memperbaiki daya ingat dan sistem motorik pasca stroke serta meregenerasi meregenerasi sel-sel baru untuk kesehatan menyeluruh. Hal ini dibuktikan dengan penelitian yang dilakukan pada pasien pasca stroke yang

dilakukan Universias Manitoba, Winnipeg, Kanada. Hasilnya menunjukkan bahwa fucoidan dalam brown seaweed  mempercepat pemulihan fungsi motorik pada minggu pertama serta memperbaiki memori. Penelitian manfaat ganggang laut coklat lainnya: 

Fucoidan dalam ganggang coklat mampu menghambat pembentukan bekuan darah sehingga menurunkan resiko terserang penyakit jantung dan stroke (Malmo University Hospital, Swedia)



Fucoidan dalam ganggang coklat mempercepat fungsi motorik pada minggu pertama dan perbaikan memori (University of Manitoba, Winnipeg-Canada)



Ganggang coklat mengubah aktifitas enzim di liver yg mengontrol metabolisme asam

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2013

Ukkie- modul saraf lbm 3 (STROKE)

Konsumsi tuna 13 kali per bulan dapat mengurangi risiko tubuh dari ischemic stroke, stroke, yaitu stroke yang disebabkan oleh kurangnya aliran darah ke otak. 3)

Sayur dan Buah-buahan Sebagian besar buah dan sayur memiliki nilai gizi dan mineral yang cukup tinggi.

Kandungan gizi tersebut sangat dibutuhkan untuk merevitalisasi sel-sel dan jaringan tubuh yang telah rusak serta meningkatkan sistem metabolisme serta sistem kekebalan didalam tubuh. Terdapat beberapa jenis buah dan sayur yang digunakan untuk mencegah dan mengobati penyakit stroke diantaranya adalah: melon, alpukat, pisang, apel, belimbing,  jambu biji, dan asparagus. Pencegahan

terjadinya

stroke

harus

dilakukan

sepanjang

masa.

Dengan

bertambahnya bertambahnya usia, kemungkinan untuk terserang stroke. Oleh k arena itu, harus diusahakan diusahakan untuk selalu mengurangi atau menghilangkan berbagai faktor resiko, terutama dengan melakukan diet dan olahraga secara teratur t eratur (Wirakusumah 2001). Selain itu, menurut Wirakusumah (2001), makanan yang dapat menolong untuk

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Ukkie- modul saraf lbm 3 (STROKE) 

2013

Vitamin E, dapat mengurangi pembentukan gumpalan darah (plak) yang dapat menyumbat arteri. Contoh sumber pangan yang mengandung vitamin E adalah taoge.



Vitamin C, dapat memperkuat dinding pembuluh darah dan mencegah terjadinya hemorrhages (keluarnya darah dari pembuluh) otak. Bahan pangan yang mengandung vitamin C antara lain jeruk, jambu biji, tomat dan lain-lain.



Sumber kalium Makanan sumber kalium seperti pisang, dapat menurunkan resiko terserangnya stroke. Diduga, asupan kalium yang memadai membuat dinding arteri lebih elastik dan normal. Selain itu, juga dapat melindungi kerusakan pembuluh darah akibat tekanan darah yang tinggi.

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Ukkie- modul saraf lbm 3 (STROKE)

2013

6. Patogenesis ? STROKE 6. Definisi Sindroma akibat lesi vaskuler ragional di batang otan . di sub kortikal atau di kortikal Pukulan mendadak 7. Macam macam stroke

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2013

Ukkie- modul saraf lbm 3 (STROKE)

sebagian besar pasien atau sebesar 83% mengalami stroke jenis ini (Misbach & Kalim 2007).  Aliran

darah ke

otak

pada

stroke

iskemik

terhenti karena

aterosklerosis

(penumpukan kolesterol pada dinding pembuluh darah) atau adanya bekuan darah yang telah menyumbat suatu pembuluh darah ke otak. Penyumbatan dapat terjadi di sepanjang  jalur arteri yang menuju ke otak. Misalnya suatu ateroma (endapan lemak) bisa terbentuk di dalam arteri karotis sehingga menyebabkan berkurangnya aliran darah. Keadaan ini sangat

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Ukkie- modul saraf lbm 3 (STROKE)

2013

neurologis yang terjadi pada waktu yang sangat singkat yaitu berkisar antara 5-20 menit atau dapat pula hingga beberapa jam, dan kemudian mengalami perbaikan secara komplit. Meskipun tidak menimbulkan keluhan apapun lagi setelah serangan, terjadinya TIA jelas merupakan hal yang perlu ditanggapi secara serius karena sekitar sepertiga penderita TIA akan mengalami serangan stroke dalam 5 tahun. Dalam keadaan lain, defisit neurologis yang telah terjadi selama 24 jam atau lebih dapat juga mengalami pemulihan secara komplit atau hampir komplit dalam beberapa hari. Keadaan ini kerap diterminologikan sebagai

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2013

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Ukkie- modul saraf lbm 3 (STROKE)

2013

antikoagulan dalam dosis yang terlalu tinggi. Gangguan perdarahan dan penggunaan antikoagulan meningkatkan resiko sekarat dari perdarahan intraserebral. Perdarahan intraserebral ini merupakan jenis stroke yang paling berbahaya. Lebih dari separuh penderita yang memiliki perdarahan yang luas, meninggal dalam beberapa hari. Penderita yang selamat biasanya kembali sadar dan sebagian fungsi otaknya kembali, karena tubuh akan menyerap sisa-sisa darah. 2.2 S u b ar ar a c h n o i d h e m o r r h a g e  (perdarahan subarakhnoid)

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Ukkie- modul saraf lbm 3 (STROKE)

2013

Hal ini penting agar semua orang mempunyai kewaspadaan yang tinggi terhadap bahaya

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2013

Ukkie- modul saraf lbm 3 (STROKE) Gejala stroke iskemik

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Ukkie- modul saraf lbm 3 (STROKE)

2013

Oklusi yang terjadi di pangkal arteri serebri media akan mengakibatkan aliran

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Ukkie- modul saraf lbm 3 (STROKE)

2013

mengakibatkan penderita mengalami kebutaan kortikal, gangguan ingatan dan

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Ukkie- modul saraf lbm 3 (STROKE)

2013

medial pedunkulus sereberi, jaras sensorik, nukleus rubra, formasio retikularis, nukleus

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