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Study Guide Neuroscience and Neurological Disorders

The seven general core competency

1. Patient care.Demonstrate capability to provide comprehensive patient care that is compassionate, appropriate, and effective for the management of health problems, promotion of health and prevention of disease in the primary health care settings.

2. Medical knowledge base.Mastery of a core medical knowledge which includes the biomedical sciences, behavioral sciences, epidemiology and statistics, clinical sciences, the social aspect of medicine and the principles of medical ethics, and apply them.

3. Clinical skill.Demonstrate capability to effectively apply clinical skills and interpret the finding in the investigation of patient.

4. Communication.Demonstrate capability to communicate effectively and interpersonally to establish rapport eith the patient, family, community at large, and professional associates, that results in effective information exchange, the creation of therapeutically and ethically sound relationship.

5. Information management.Demonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to patient’s specific problem, and maintening records of his or her practice for analysis and improvement.

6. Professionalism.Demonstrate a commitment to carrying out professional responsibilities and to personal probity, a dherence to ethical principles, sensitivity to a diverse patient population, and commintment to carrying out continual-self-evaluation of his or her professional standard and competence.

7. Community-based and health system-based practice.Demonstrate awareness and responsiveness to large contex and system of health care, and ability to effectively use system resources for optimal patient care.

1Faculty of Medicine Udayana University, DME


~ LECTURERS ~

NO NAME DEPARTMENT PHONE

1 Prof. Dr. dr. I N. Mangku Karmaya, M.Repro, PA(K) Anatomy 0811387105

2 dr. I Dewa Ayu Inten Dwi Primayanti, M.Biomed Fisiology 081337761299

3 dr. I Wayan Sugiritama, M.Kes Histology 08164732743

4 Dr. dr. I Made Jawi, M.Kes Pharmacology 08179787972

5 dr. A.A.B.N. Nuartha, Sp.S(K) Neurology 08179782240

6 Dr. dr. DPG. Purwa Samatra, Sp.S(K) Neurology 08123918731

7 dr. I Made Oka Adnyana, Sp.S(K) Neurology 0817347697

8 dr. Meidiary, Sp.S Neurology 08123616763

9 dr. Widyastuti, Sp.S Neurology 08123634110

10 Dr. dr. Thomas Eko Purwata, Sp.S(K) Neurology 08123948477

11 Dr. dr. Anna Marita Gelgel, Sp.S(K) Neurology 08123870038

12 dr. Susilawathi, Sp.S Neurology 08124690137

13 dr. I Komang Arimbawa, Sp.S Neurology 081338226892

14 dr. I. A. Dayu Sriwijayanti, Sp.S Neurology 081337667939

15 dr. Kumara Tini, Sp.S., FINS Neurology 081238701081

16 Prof. DR. dr. Sri Maliawan, Sp.BS Surgery 0811398466

17 Dr. dr. Nyoman Golden, Sp.BS Surgery 0811380037

18 dr. Tjok. Gd. Bagus Mahadewa, M.Kes., Sp.BS Surgery 0818484654

19 dr. Wayan Niryana, Sp.BS Surgery 08179201958

20 dr. Putu Pramana Suarjaya, Sp.An., M.Kes Anasthesi 0811394811

21 dr. Widhiasih, Sp.Rad Radiology 081916442626

22 dr. Ni Putu Sriwidnyani, Sp.PA Anatomy Phatology 081337115012

23 Dr. dr. A.A. Ngurah Subawa, M.Si., Sp.PK Clinical Phatology 08155735034

24 dr. Muliani, M. Biomed Anatomy 085103043575



FACILITATORS ~Regular Class (Class A)

No Name Group Departement PhoneVenue

(3rdfloor)

1 dr. I Gede Putu Supadmanaba, S.Ked 1 Biochemistry 082146558748 3rd floor: R.3.09

2 Ni Putu Wardani, Sp.An, M.Biomed 2 DME 081337660988 3rd floor: R.3.10

3 dr. Putu Ariastuti, MPH 3 Public Health 0818560008 3rd floor: R.3.11

4 dr. Ida Bagus Sutha, Sp.P-K 4 Pulmonology 08123990362 3rd floor: R.3.12

5 dr. Muliani, M.Biomed 5 Anatomy 085103043575 3rd floor: R.3.13

6 dr. Ni Made Ari Suryathi, M.Biomed, Sp.M 6 Opthalmology 085253651928 3rd floor: R.3.14

7 dr.Ni Luh Putu Ratih Vibriyanti Karna,Sp.KK 7 Dermatology 081337808844 3rd floor: R.3.15

8 dr. Putu Gede Sudira, Sp.S 8 DME 081805633997 3rd floor: R.3.16

9 dr. Agung Nova Mahendra, M.Sc 9 Pharmacology 087861030195 3rd floor: R.3.17

10 dr. Ari Andayani, Sp.M 10 Opthalmology 08113803666 3rd floor: R.3.19

English Class (Class B)

No Name Group Departement PhoneVenue

(3rdfloor)

1 dr. I G N Wien Aryana, Sp.OT 1 Orthopaedi 0811385263 3rd floor: R.3.09

2 Prof.dr. I Dw Pt Sutjana, PFK, M.Erg 2 Fisiology 08123924477 3rd floor: R.3.10

3 dr. Ida Ayu Kusuma Wardani, Sp.KJ, MARS 3 Psychiatry 08123813831 3rd floor: R.3.11

4 Dr.rer.Nat. dr. Ni Nyoman Ayu Dewi, M.Si 4 Biochemistry 081337141506 3rd floor: R.3.12

5 Dr.dr. I Made Muliarta, M.Kes 5 Fisiology 081338505350 3rd floor: R.3.13

6 dr. I G P Suka Aryana, Sp.PD-Kger-FINASIM 6 Interna 08164724600 3rd floor:

R.3.14

7 Dr. dr. Made Sudarmaja, M.Kes 7 Parasitology 08123953945 3rd floor: R.3.15

8 Dr.dr. Ni Nyoman Sri Budayanti, Sp.MK(K) 8 Microbiology 08553711398 3rd floor: R.3.16

9 dr. I Wayan Sugiritama, M.Kes 9 Histology 08164732743 3rd floor: R.3.17

10 dr. I Made Susila Utama, Sp.PD-KPTI 10 Interna 08123815025 3rd floor: R.3.19



Neuroscience Basic Semester IVTopic and Schedule Reguar and English Class

Day/Date

Activity Class B Class A Venues Conveyer

1May 16th

2016

Introduction lecture. Refleks segmental, intersegmental dan suprasegmental.

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

dr. Kumara Tini, Sp.S, FINS / Prof.

Mangku

Facilitators

Prof. Mangku2

May 17th

2016

Lecture Koordinasi pergerakan dan keseimbangan.

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

dr. Muliani

Facilitators

dr. Muliani3

May 18th

2016

Lecture: Meninges, vaskularisasi dan liquor cerebrospinalis.

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

Prof. Mangku

Facilitators

Prof. Mangku4 Lecture. 08.00-09.00 09.00-10.00 Class room dr. Inten



May 19th

2016 Individual Learning

SGD

Break

SP/Self Assessment

Plenary

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

-

Discussion room

-

-

Class room

Facilitators

dr. Inten

5May 20th

2016

Lecture

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

dr. Inten

Facilitators

dr. Inten6

May 23th

2016

Lecture

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

dr. Sugiritama dr. Sriwidyani

Facilitators

dr. Sugiritama dr. Sriwidyani

7May 24th

2016

Lecture

Individual Learning

SGD

Break

SP/Self Assessment

Plenary

08.00-09.00

09.00-10.30

10.30-12.00

12.00-12.30

12.30-14.00

14.00-15.00

09.00-10.00

12.00-13.30

13.30-15.00

11.30-12.00

10.00-11.30

15.00-16.00

Class room

-

Discussion room

-

-

Class room

dr. Subawa .dr. Jawi

Facilitators

dr. Subawa .dr. Jawi

8May 25th

2016Evaluation 09.00-11.00 09.00-11.00 Class room LECTURER,

FACILITATORS.



LEARNING PROGRAM

Day 1st

Bagian Anatomi FK UNUD

ABSTRAK Setiap mahluk hidup membutuhkan suplai informasi tentang apa yang terjadi di luar maupun di

dalam dirinya. Informasi ini penting untuk direspon secara sepadan dan integral, sehingga dapat mempertahankan kelangsungan hidupnya. Untuk keperluan semacam ini, maka tubuh mengembangkan sejenis sel yang berdiferensiasi menjadi sangat special yaitu sel saraf (neuron).

Sel-sel saraf bebentuk khusus dan memiliki sifat peka terhadap rangsangan/ stimulus (eksitabilitas atau iritabilitas) dan dapat mengantarkan akibat-akibat rangsangan tersebut secara amat sempurna (konduktivitas). Dengan demikian sel saraf dapat berperan sebagai penerima rangsang (aferen/ sensorik) dan menghantarkan rangsang ke organ-organ efektor (eferen/ motorik). Penghantaran impuls ini hamper semuanya terjadi melalui suatu susunan saraf pusat yang menghubungkan saraf sensorik dan motorik itu.

Sel-sel saraf bersama-sama dengan sel-sel penunjang yang disebut neuroglia, dilayani oleh pembuluh-pembuluh darah. Ketiga komponen itu, sel saraf, neuroglia dan pembuluh darah bersama-sama membentuk jaringan saraf.

Meskipun tampak berserakan di seluruh tubuh, sel-sel saraf terorganisir dalam dua susunan yaitu Susunan Saraf Perifer dan Susunan Saraf Pusat. Susunan Saraf Perifer terdiri dari (a) nervi craniales, (b) nervi spinals (nervi segmentales) dan (c) Susunan Saraf Visceral. Kelompok (a) dan (b) dikenal sebagai saraf cerebrospinal atau craniospinal sedangkan (c) Susunan Saraf Visceral terdiri atas susunan saraf visceral aferen dan susunan saraf visceral eferen. Yang terakhir ini juga disebut sususanan saraf otonom atau susunan saraf vegetative.

Komponen Susunan Saraf Pusat terdiri dari otak (ensefalon, yang dibangun oleh prosencephalon, mesencephalon dan rhombencefalon) dan medulla spinalis. Komponen-komponen ini dapat dipelajari dari skema buku Neuroanatomia (Elias Sukardi, halaman 3 dan 4).Tujuan Umum: memahami dasar-dasar organisasi struktural SSP dan SST sebagai landasan studi klinis dan penelitian di bidang neurologi.

Tujuan khusus:1. Mampu menggambarkan topografi dan organisasi structural otak dan medulla spinalis2. Mampu memahami anatomi fungsional sensorik dan motorik dan integrasinya dalam mengatur

gerakan reflex dan gerakan yang terkoordinir yang melibatkan SST dan SSP pada level rendah sampai pusat-pusat lebih tinggi.

3. Mampu memahami prinsip-prinsip suplai darah, drainase vena dan aliran liquor serta menyimpulkan dampak dari ganggguan fungsi ini.

4. Manpu menjelaskan terjadinya malformasi pada sistem saraf.

Topik Kuliah1. Refleks Segmental, intersegmental dan suprasegmental

Subtopik: morfologi sel saraf, aspek fungsional saraf, akson dan neurotransmitter, medulla spinalis, anatomi fungsional nervi spinals dan nervi craniales dan batang otak

2. Koordinasi pergerakan dan keseimbangan



Subtopik: tractus ascendentes(sensorik) dan desendentes (motorik), batang otak, formatio reticularis, cerebellum, telencephalon, cortex cerebri, diencephalon, ganglia basalia, jalur saraf penglihatan, pendengaran, keseimbangan dan pembau

3. Meninges, vaskularisasi dan liquor cerebrospinalisSubtopik: meninges, vaskularisasi SSP, sirkulasi liquor cerebrospinalis, garis besar pertumbuhan dan perkembangan SSP.

Learning objective Topik Kuliah 1: Refleks Segmental, intersegmental dan suprasegmental1. Menjelaskan anatomi fungsional system saraf secara umum2. Mengggambarkan berbagai bentuk sel saraf dan bagian-bagiannya3. Menjelaskan jenis sel saraf berdasarkan sifatnya 4. Menjelaskan sifat axon, selubung myelin dan mekanisme pengantaran gelombang depolarisasi

dan repolarisasi5. Memahami jenis sinaps, jenis-jenis neurotransmitter dan mekanisme pengantaran impuls

melalui daerah sinapsis.6. Membedakan SSP dan SST dalam hal lokasi, fungsi dan susunan histologik umum7. Menjelaskan komponen utama suatu lengkung reflex yang paling sederhana8. Menjelaskan macam rangsangan dan macam reseptornya.9. Menjelaskan tentang Susunan Saraf Otonom (SSO)10. Menjelaskan perjalanan saraf sensoris dari perifer sampai ke SSP dan saraf motoris dari SSP

ke perifer. 11. Memahami susunan umum tractus ascendentes dan descendentes dalam SSP12. Menjelaskan anatomi nervi spinals dan nervi craniales beserta sifat-sifatnya13. Menjelaskan perjalanan dan struktur yang terlibat dalam reflex segmental, intersegmental dan

supra segmental.

Kasus 1.Seorang pasien laki-laki dewasa datang dengan keluhan tidak bisa menggerakkan kaki kanannya. Kulit daerah tersebut juga merasa tebal. Derita ini dimulai sesudah jatuh dari pohon kelapa. Pada pemeriksaan neurologis ditemukan kekuatan otot kaki menurun, tonusnya berkurang dan sensasi negatip. Reflex patella juga negatip. Dokter menduga adanya kerusakan plexus lumbosakralis yang melayani kakinya.

1. Gambarkan bagan sebuah sel saraf dan sebutkan bagian-bagian serta fungsi dari masing-masing bagian itu

2. Gambarkan jenis-jenis sinaps dan jelaskan mekanisme penghantaran impuls pada sel saraf dan pada sinaps

3. Gambarkan bagan saraf spinal, percabangan dan sifat-sifatnya4. Jelaskan anatomi dan fungsional nervi craniales5. Pasien tidak bisa menggerakkan kaki dan kehilangan sensasi pada kulit kaki. Jelaskan jenis

saraf berdasarkan sifatnya dan nama jenis-jenis reseptor

Kasus 2. Suatu ketika anda berjalan dengan kaki telanjang. Tiba-tiba saja anda tersenta mengangkat kaki anda. Ternyata anda menginjak puntung rokok yang lagi menyala. Anda juga tidak sadar kalau anda juga menggerakkan tangan anda. Pada saat itu juga muka anda pucat dan jantung berdebar-debar.

1. Gambarkan dan jelaskan bagan sebuah lengkung reflex. Jelaskan mengapa secara reflex tangan anda ikut bergerak.



2. Jelaskan perjalanan saraf sensoris dan posisinya dalam SSP sampai sensasi nyeri itu diterima otak

3. Jelaskan perjalanan saraf motorik dan posisinya dalam SSP dari pusat pergerakan di otak sampai kepada efektor (otot skelet)

4. Jelaskan tentang Upper Motor Neuron (UMN) dan Lower Motor Neuron (LMN) serta akibat yang timbul dari kerusakan kedua jenis saraf ini.

5. Gambarkan bagan medulla spinalis dan jelaskan aspek fungsional bagian-bagiannya.

ABSTRACTEvery living thing needs a steady supply of information about what is going on outside and

inside himself. This information is important to respond commensurately and integral, so it can maintain its viability. For the purposes of this kind, the body develops a type of cells that differentiate into that very special nerve cells (neurons).

Nerve cells specialized shaped and has a sensitive nature to the stimulus (excitability or irritability) and can deliver the effects of these stimuli are so perfect (conductivity). Thus the nerve cells can act as a receiver excitatory (afferent / sensoric) and deliver stimuli to the effector organs (efferent / motoric). This impulse conduction almost everything happens through a central nervous system that connect the sensoric and motoric nerves.

Nerve cells together with supporting cells called neuroglia, served by blood vessels. The three component of the nerve cells, neuroglia and blood vessels together form a neural tissue.

Although the entire bodies were scattered by the nerve cells, but they are well organized into two trees Peripheral and Centran Nervous System. Peripheral Nervous Structure consists of (a) nervi craniales, (b) nervi spinals (nervi segmentales) and (c) Visceral Nerve System. The group (a) and (b) is known as cerebrospinal nerves or craniospinal while (c) Visceral nervous system consist of visceral afferent and efferent. The latter is also called the autonomic nervous sususanan or vegetative nervous system.

Components CNS consists of the brain (ensefalon, built by prosencephalon, mesencephalon and rhombencefalon) and spinal cord. These components can be learned from books scheme Neuroanatomia (Elias Sukardi, pages 3 and 4).

General Goal: to understand the basics structural organization of SSP and SST as the basis for clinical studies and research in the neurology field.Specific Goals:

1. Being able to describe the topography and the structural organization of the brain and spinal cord

2. Be able to understand the functional anatomy of sensory and motor and its integration in regulating reflex movements and coordinated movement involving PNS and CNS at a low level until the higher centers.

3. Be able to understand the principles of the blood supply, venous drainage and flow of liquor and concluded the impact of the disruption this function.

4. Be able to explain the occurrence of malformations in the nervous system.

Lecture topics:1. Segmental reflex, intersegmental and suprasegmental.

Subtopic: nerve cell morphology, functional aspects nerve axons and neurotransmitter, spinal cord, functional anatomy and nervi nervi spinals craniales and brainstem

2. Coordination of movement and balance



Subtopic: tractus ascendentes (sensoris) and desendentes (motoric), brainstem, formatio reticularis, cerebellum, telencephalon, cerebral cortex, diencephalon, ganglia basalia, neural pathways of vision, hearing, balance and smell

3. The meninges, vascularization and liquor cerebrospinalisSubtopic: meninges, CNS vascularization, the circulation of liquor cerebrospinalis, outline growth and development of the CNS.

Learning objective Lecture Topic 1: Segmental reflex, intersegmental and suprasegmental1. Describe the functional anatomy of the nervous system in general2. Draw various forms of nerve cell and its parts3. Describe the types of nerve cells by their nature4. Explain the nature of axons, the myelin sheath and delivery mechanisms wave of depolarization

and repolarization5. Understand the type of synapse, neurotransmitters and other types of delivery mechanisms

impulses through synapses area6. Distinguish CNS and PNS in terms of location, function and common histological composition7. Describe the main components of a simplest reflex arc 8. Describe the types of stimulation and wide receptors.9. Describe the Autonomous Nervous System (SSO)10. Describe the journey of sensory nerves of the peripheral to the CNS and motor nerves of the

CNS to the periphery.\Understand the general arrangement tractus ascendentes and descendentes in the CNS

11. Explaining anatomy of nervi spinales and nervi craniales along its properties12. Describe the journey and structures involved in the reflex segmental, intersegmental and

segmental supra.

Case 1.An adult male patient came with complaints could not move his right leg. The skin of the area also felt thick. This condition starts after falling from a palm tree. On neurological examination found decreased leg muscle strength, reduced muscle tone and negative sensations. Patellar Reflex also negative. Doctors suspect the lumbosacral plexus damage that serves legs.

1. Draw a chart of a nerve cell and identify the parts and functions of each part 2. Describe the types of synapses and explain the mechanism of impulse conduction in nerve

cells and the synapses3. Draw a chart of spinal nerves, components and its properties4. Explain the anatomical and functional aspect of nervi craniales5. The patient can not move his right leg and loss of sensation in the skin of the foot. Describe 6. the type of nerve by its nature and name the types of receptors

Case 2.Once you walk barefoot. Suddenly you lift up your foot. It turns out you step on the rest of burning cigarette. You also do not realize that you also move your hands. At that moment, you face pale and heart palpitations.

1. Describe and explain the chart a reflex arc. Explain why you joined hands reflex move.2. Describe the journey of sensory nerves in the CNS and its position until pain sensation received

by the brain 3. Explain the trip of the motor nerves in the CNS and its the position from the center of the

movement in the brain to the effector (skeletal muscle)



4. Explain the Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) as well as the consequences arising from these two types of damage.

5. Draw a chart of the spinal cord and explain the functional aspects of its parts.

Day 2nd


Learning Objective Topik Kuliah 2: Koordinasi pergerakan dan keseimbangan1. Menjelaskan peran batang otak dalam menghantarkan impuls motorik dan sensorik2. Menjelaskan struktur, peran dan fungsi formatio reticularis3. Menjelaskan arsitektur struktur cerebellum dan hubungan aferen dan eferen dengan nuclei di

luar cerebellum4. Menjelaskan topografi pusat-pusat fungsional dan hubungan fungsional pusat-pusat ini pada

cortex cerebri dikaitkan dengan sulci dan gyri dan area Brodmann.5. Menjelaskan jalur koordinasi pusat motorik cortex cerebri dengan nuclei subcorticalis dan

pusat-pusat motorik di batang otak sampai medulla spinalis6. Menjelaskan pusat-pusat yang berkaitan dengan emosi7. Menjelaskan jalur saraf yang mengendalikan keseimbangan8. Menjelaskan jalur saraf penglihatan, pendengaran dan pembauan.

Kasus 1.Seorang ibu setengah baya diantar keluarganya ke instalasi gawat darurat karena tiba-tiba rebah, lidah kelu dan lumpuh lengan dan kaki kanannya. Si ibu adalah seorang temperamental dan memiliki riwayat tekanan darah tinggi. Diduga si ibu mengalami stroke. Jelaskan posisi pusat-pusat fungsional cortex cerebri menurut Brodmann dan hubungannya antar pusat-pusat tersebut.

1. Jelaskan lapisan-lapisan cortex cerebri dan jelaskan sirkuit neuron di dalamnya2. Jelaskan jalur saraf motorik dari cortex cerebri sampai ke saraf cranial dan spinal3. Jelaskan peran ganglia basalia dalam koordinasi pergerakan4. Jelaskan anatomi susunan saraf pyramidal dan extrapyramidal serta konsekuensi dan

kerusakan kedua system ini5. Jelaskan pusat-pusat neuron yang mengatur emosi

Kasus 2Sesudah sebulan dirawat, pasien laki-laki remaja yang mengalami trauma kapitis mengalami mata kabur, sempoyongan, pendengaran telinga kiri menurun dan rasa-rasa bau berkurang.

1. Jelaskan susunan arkitektur cerebellum serta jelaskan sirkuit neuron di dalamnya2. Jelaskan hubungan-hubungan cerebelulum dengan nuclei extra cerebellar dalam pengaturan

pergerakan dan keseimbangan3. Gambarkan perjalanan jaras neuron penglihatan sampai tiba di pusat penglihatan cortex

cerebri dan jelaskan kelainan akibat kerusakan jaras penglihatan dalam perjalanannya menuju otak.

4. Jelaskan perjalanan saraf pendengaran sampai ke pusat pendengaran5. Jelaskan perjalanan saraf pembau sampai ke pusat pembauan.



Learning objective Lecture Topic 2: Coordination of movement and balance1. Explain the role of the brain stem in delivering sensory and motor impulses2. Describe the structure, role and functions of formatio reticularis3. Describe the architectural structure of the cerebellum and its relationship with the afferent and

defferent nuclei outside the cerebellum.4. Describe the topography of the functional centers and functional relationships of these centers

in the cerebral cortex associated with sulci and gyri and Brodmann area.5. Explain the coordination center lane motor cortex cerebri with subcorticalis nuclei and motor

centers in the brain stem to the spinal cord6. Explain the centers related to emotions7. Describe the neural pathways that control balance8. Explain the neural pathways of vision, hearing and smelling.

Case 1.A middle-aged mother escorted his family to the emergency room due to a sudden fall, tongue-tied and paralyzed of her right arm and leg. The mother is a temperamental and had a history of high blood pressure. Allegedly the mother suffered a stroke.

1. Describe the layers of cerebral cortex and explain the neural circuits in it2. Explain the motor nerve pathways from the cerebral cortex to the cranial and spinal nerves3. Describe the role ganglia basalia in coordinating the movement4. Explain the anatomy of the pyramidal and extrapyramidal nervous system as well as the

consequences and damage to both this system5. Describe the centers of neurons that regulate emotion

Case 2After a month being treated, the patient adolescent male who got head injury suffered blurry eyes, staggered, declining left ear hearing and reduced odor flavors.

1. Describe the composition of architecture of the cerebellum and explain the neural circuits in it.2. Explain the relationships of the cerebelum with extra cerebellar nuclei in regulating the

movement and balance3. Describe the vision neuron pathways trip until arriving at the visual center cerebral cortex and

explain the vision pathway abnormalities due to damage on its way to the brain.4. Describe the auditory nerve trip up to the hearing center!5. Describe the smell journey to the center nerve of smelling!

Day 3rd


Learning objective Topik Kuliah 3: Meninges, vaskularisasi dan liquor cerebrospinalis1. Menjelaskan dasar-dasar pelapisan SSP dan derivatnya (pembentukan falx cerebri, tentorium

cerebelli, diaphragm sellae, falx cerbelli dan sinus duramatris).2. Menjelaskan dasar-dasar vaskularisasi SSP dan SST3. Menjelaskan regionalisasi vaskularisasi otak.4. Menjelaskan sirkulasi liquor cerbri5. Menjelaskan garis besar pertumbuhan dan perkembangan SSP6. Menjelaskan kelainan congenital SSP.



Kasus 1Seorang anak usia 3 tahun datang dengan panas tinggi dan kejang. Pada pemeriksaan ditemukan adanya kaku kuduk. Diduga si anak menderita meningitis

1. Sebutkan semua lapisan meningen dan derivatnya yang membungkus SSP 2. Sebutkan nama ruang di antara lapisan-lapisan meninges3. Jelaskan hubungan antar ruang tersebut4. Jelaskan perjalanan aliran liquor serebrospinalis5. Jelaskan hubungan liquor serebrospinalis dengan pembuluih darah

Kasus 2Seorang pria direktur bank sesudah rapat yang melelahkan tiba-tiba ambruk di kantornya. Ambulans segera membawanya ke rumah sakit scanning kepa menunjukkan adanaya perdarah pada capsula interna kanan. Sang direktur mengalami hemorrhagic stroke.

1. Jelaskan dasar-dasar vaskularisasi SSP2. Jelaskan tentang Circulus Arterosus Cerebri (Willis). pembuluh darah yang melayani otak dan

daerah layanannya3. Gambarkan dan jelaskan diagram arteriae yang melayani medulla spinalis 4. Jelaskan terjadinya hydrocephalus dan spina bifida.

Learning objective Lecture Topic 3: The meninges, vascularization and liquor cerebrospinalis.Describe the basics coating of CNS and its derivatives (formation of falx cerebri, tentorium cerebelli, diaphragm sellae, falx cerbelli and sinus duramatris).

1. Explain the basics of vascularization CNS and PNS2. Explain the regionalization vascularisation of the brain.3. Explain the circulation of liquor cerbri4. Explain the outline of growth and development of the SSP5. Explain the SSP congenital abnormalities.

Case 1 A child aged 3 years comes with high fever and seizures. On examination discovered the existence of a stiff neck. The child suspected suffering from meningitis

1. List all layers of the meninges and its derivatives that wraps CNS2. Name of the space between the layers of the meninges3. Describe the relationship between space4. Explain the trip flow of cerebrospinal liquor5. Describe the relationship liquor cerebrospinal with blood pembuluih

Case 2A man bank director after exhausting meetings suddenly collapsed in his office. An ambulance rushed him to hospital. Head scanning showed bleeding of the right internal capsule. The director suffering hemorrhagic stroke

1. Explain the basics of vascularization of CAN2. Tell about Circulus Arterosus Cerebri (Willis). 3. Describe blood vessels serving the brain and its service area4. Describe and explain diagrams that serve the spinal cord arteriae5. Describe the occurrence of hydrocephalus and spina bifida.



Day 4th

NEUROPHYSIOLOGYdr. I Dewa Ayu Inten Dwi Primayanti, M. Biomed.

AIMS :To comprehend the general functions of the nervous system include sensory detection, information processing and responsible for controlling a variety of bodily activities such as contraction of muscle and secretion of gland.

LEARNING OUTCOMES :Apply its concepts and principles in the approach of patient with neurological disorders

CURRICULUM CONTENTS :I. GENERAL DESIGN OF THE NERVOUS SYSTEM (NS)

1. Cells of the NS (Neurone and Neuroglia)2. Sensory division of the NS – sensory receptors3. Motor division – the effectors4. Processing of information – memory5. Memory storage

II. MAJOR LEVEL OF THE CNS1. Cortical level2. Subcortical level3. Spinal cord level

III. CENTRAL NERVOUS SYSTEM SYNAPSES1. Types of synapses2. Physiologic anatomy of the synapses3. Chemical substances that function at synaptic transmission4. Electrical events during neuronal excitation and inhibition5. Special function of dendrites in exciting neurons6. Relation of state of excitation - the neuron to rate of firing7. Some special characteristics of synaptic transmission.

ABSTRACTI. The nervous system (NS) includes both sensory (input) and motor (output) system

interconnected by complex intgrative mechanisms.The nervous system divided into the central nervous system (CNS) and the

peripheral nervous system (PNS)a. The CNS includes the brain and and spinal cord, which contain nuclei and tracts.

Nuclei are grouping of neuron cell bodies within the CNS. Tract are grouping nerve fibers that interconnect regions of the CNS.

b. The PNS consists of nerves, ganglia and nerve plexuses. Nerve is cablelike collection of many axons, may be mixed (contains both sensory and motor fibers). Ganglia is grouping of neuron cell bodies located outside the CNS

1. Cells of the nervous system The NS is composed primarily of two cell types are found in CNS & PNS

a. The neuron is the basic structural and functional unit of the NS, which typically consist of a cell body (soma), several dendrites, and a single axon. Neuron structure is related



to function, which have receptive and integrative zone (dendrite and cell body), trigger zone (axon hillock), and conductive region (axon) especially in terminal end of axon has secretive synaptic transmitter.Electrochemical activity in neuron include- Membrane potential: polarization, depolarization, repolarization, hyperpolarization.- Graded electrogenesis: i.e graded potential, receptor potential, EPSP, IPSP.- Site of origin of conducted impuls (action potential), all or none transmission,

incoming signal in terminal end of the axon as trigger to secreting transmitter synaptic

Neuron communicate with muscle, gland, and other neurons at junction its called neuromyal junction, neuroglandular, and synapses. Synapses are found in dendrite, soma, and axon (axodendrtic, axosomatic, axoaxonic synapses).

b. The four major types of glial cells (Neuroglia ) in the CNS are astrocytes, oligodendrocytes, microglia, and ependymal cells. Glial cells help support the neuron both physically and metabolically. For instance function of the astrocytes as glue, scaffold, establishing blood brain barrier, repair brain injuries and neural scar formation, take up glutamate and GABA, take up excess K+ ECS, and enhance synaptic formation and to strengthen synaptic transmission. oligodendrocytes form myelin sheath, line internal cavity of the CNS contribute to the formation CSF (ependymal cells), microglia as scavenger.

c. Synaptic transmission involves release of neurotransmitter from the presynaptic cell, diffusion of neurotransmitter across the synaptic cleft and binding of neurotransmitter to receptors on the postsynaptic cell. It ends when the neurotransmitter dissociates from the receptor and is removed from the synaptic cleft.

2. Much of the activity in the NS arises from mechanism that stimulate sensory receptor located at the distal termination of sensory neuron. Signal travel over peripheral nerves to reach the spinal cord and are then transmitted throughout the brain. Incoming sensory massages are processed and integrative with information stored in various pools of neurons such that the resulting signals can be used to generate appopriate motor response

II. SELF – STUDY , ESSAY QUESTION

1. Describe the structure of neuron and explain significance of its principal regions.2. Classify neurons on the basis of their structure and function.3. Describe the location, the major types, and functions of the supporting cells.4. Explain how the graded potential and action potential differ5. Define polarization, depolarization, repolarization and hyperpolarization.6. Explain the actions of voltage regulated Na+ and K+ channels and describe the event that

occur during the production of an action potential.7. Explain how action potentials are regenerated a long myelinated and non myelinated

axon..8. Describe the events that occur in the interval between the electrical excitation of axon and

the release of neurotransmitter.9. Compare the characteristics of EPSPs and action potential10. Explain the synaptic transmission exhibits special characteristic11. Explain how sensory receptors are categorizeds. Give examples of functional of functional

categories and explain how tonic and phasic receptors differ 12. Describe the classification of the sensory division – sensory receptors.



13. Give examples of different types of cutaneous receptors (somatosensory receptors) and describe the neural pathways for the cutaneous senses

14. Explain how the mechanical energy is tranduced/ converted into nerve impulses by the organ Corti and how pitch perception is accomplished.

15. Give examples the following modalities are tested : sense of pain, temperatur, touch, vibration, and sense of positition

16. Distinguish between and compare monosynaptic and polysynaptic reflexes.

III. Scenario / case studya) A man falls into deep sleep with one arm under his head. This arm is paralyzed when he

awakens, but it tingles, and pain sensation in it is still intact1. What is the reason for the loss of the motor function without loss of pain sensation is

that in the nerves to his arm2. What is a thorough general physical examination should be made in this case.3. Which one of the sensory test should be done4. Which one of the reflex test should be done5. Describe general physical examination should always be done in motor system of this

caseb) Arthritis is common painfull condition caused by inflammation of one or more joints.

1. Why the joint to developed hyperalgesia in this case?c) In some diseases of the NS, myelin may be lost over one or more internodes of many axons

without interruption of the axon. For instance Guilain – Barre syndrome, diphtheria, and multple sclerosis1. Why the conduction of nerve impulses may be slowed or blocked.

d) 74-year-old man suddenly found that he couldnot move his left arm and leg.Examination in the emergency departement demonstrated weakness in the left arm and leg, especially in the distal part of these extremities.The patient also had difficulty in using the muscles of his lower face, and the left side of his tongue was not as strong as the right side. Babinski’s sign was present on the left side. In an examination 1 month later, the distribution of weakness had not changed, although the weakness was not quite as profound. The left biceps, triceps, patellar, and ankle jerk reflexes were markedly increase, and there was ankle clonus on the left. The ability of the patient to recognize tactile and vibratory stimuli was reduced on the left side of the face and body and proprioception was impaired in the left arm and leg.

1. Which part of the NS is most likely affected by the stroke? (spinal cord on the left, precentral and post central gyri on the right, internal capsul on the right, cerebellar on the left, BG on the right.)

2. Which of the following provides evidence indicating that the paralysis is of the spastic type?

Day 5th

NEUROPHYSIOLOGYdr. I Dewa Ayu Inten Dwi Primayanti, M. Biomed.

I. ABSTRACT



1. The motor division of the NS as responsible for controlling a variety of bodily activities such contraction of muscle and secretion by exocrine and endocrine glands. Actually, only a relatively small proportion of the sensory input receive by the brain is use to generate an immediate motor response. Much of it is discarded as irrelevant to the function at hand. Sensory input can be stored in the form of memory. Information stored as memory can become part of the processing mechanism used to manage subsequent sensory input. The brain compare new sensory experiences with those stored and in this way develops successfull strategies to form a motor output.

II. SELF – STUDY , ESSAY QUESTION1. Give examples of strech reflexes, including those that are frequently tested clinically.2. Describe the muscle spindles and analyze their function as part of feed back system that

maintains muscle force3. Describe the Golgi tendon organs and analyze their function as part of feed-back system

that maintains muscle force4. Define reciprocal innervation, inverse stretch reflex, clonus and lengthening reaction5. Describe in general terms how posture and movement are regulated6. Discuss the function of the cerebral cortex, cerebellum, basal ganglia, and corticospinal

and corticobulbar tracts in skilled voluntary movement7. Describe the postural reflexes that are integrated in the medulla oblongata, the pons, the

midbrain, in the cerebral cortex.8. What is meant by the terms upper motor neuron and lower motor neuron? Contrast the

effects of lower motor neuron lesions with those of lesions affecting each of types of upper motor neurons.

9. What is the Babinski sign? What is it physiologic and pathologic significance?

III. Scenario / case studya) 78-year-old man suddenly developed a right sided hemiplegia. He was unable to give a

satisfactory history because the only words that he could speake were curse words. However, he did not his had approciately response to questions

1. Which part of the brain produced the speech disorder in this patient?2. What other neurological deficit in this patient likely to have?

DAY 6th

HistologyHISTOLOGICAL STRUCTURE OF NERVOUS SYSTEM

Dr. Wayan Sugiritama, M.Kes

Abstract:Anatomically, the nervous system is divided into the central nervous system (CNS), consisting

of the brain and the spinal cord; and the peripheral nervous system(PNS), composed of nerve fibers and small aggregates of nerve cells called nerve ganglia. Structurally, nerve tissue consists of two cell types: nerve cells, or neurons, which usually show numerous long processes; and several types of glial cells, which have short processes.

The brain contains about 1012 neurons, each of which has a cell process (axon and dendrite) through which it establishes contacts with hundreds of other neurons. The spaces between neurons



are occupied by neuroglia which have short processes, support and protect neurons, and participate in neural activity, neural nutrition, and the defense processes of the CNS

Brain and spinal cord are covered by three layers of connective tissue, meningens. The outermost layer is the dura mater, the innermost is the pia mater, and an intermediate layer between these is the arachnoid.

The nerve of PNS consists of varying numbers of myelinated and unmyelinated axons originating from neurons located in the brain, spinal cord, or ganglia. Functionally, the PNS is divided into a sensory (afferent) component, which receives and transmits impulses to the CNS for processing, and a motor (efferent) component, which originates in the CNS and transmits impulses to effector organs throughout the body. The motor component is further subdivided as: somatic system and autonomic system.

A major function of the CNS is to receive sensory stimuli from various parts of the body and to analyze this information and respond by generating signals that are transmitted over PNS to initiate and integrate muscular, secretory, and other activities in the body. The function of the CNS is not limited to integration of information from the periphery, it is also engaged in less well understood endogenous neural activity that underlies consciousness, memory, reasoning, and regulation of behavior.

Learning Tasks:Trigger Case 1:A 22-year-old male had a severe, traumatic injury on his head and lower back after a motorcycle accident. He referred to the hospital in unconscious state. There was large hematoma on his head and abrasion on lower back. A CT-Scan was done and found subdural hematoma and brain edema. The surgical was done to safe his life. When the patient conscious he cannot feel and move both of his leg. Neurological examination found there was decreased of motoric and sensory function on his leg. Tasks:

1. On the above case, the patients had cerebral edema, please explain the microscopic structure of the brain and find the differences between the cerebrum and the cerebellum!

2. When the accident occurred, meninges is one structure that protects the brain from injury. Please explain the structure of the meninges and it’s clinical importance!

3. Decreased of motoric and sensory function on patient’s leg may caused by spinal cord injury, please explain its structure !

4. On the accident, peripheral nerve system (PNS) may have injured, explain the microscopic structure of Peripheral Nervous system (PNS), and its classification!

5. After an injury is usually followed by a healing process, please explain the healing process in the central nervous system and peripheral nervous system.

Trigger Case 2:A one-year-old boy referred to the neurologist with enlargement of the head, vomiting and fatigue. On examination the doctor found decreased of muscular function. A lumbar puncture was done to measure the intracranial pressure and collect the sample of cerebrospinal fluid (CSF). There was an increase of intracranial pressure and the composition of CSF was normal. He was diagnosed with hydrocephalus. Tasks:

1. On the above case, the patients had increased of intracranial pressure that may be caused by the accumulation of CSF, please explain the structure that produces CSF, the CSF production process and it’s absorption!

2. Explain the role of the blood-CSF barrier in maintained the chemical stability of the CSF!



3. Describe the structure of neuroglial cell which is have a role in circulation of CSF!

Trigger Case 3A two-year-old girl admitted to the hospital with high body temperature followed by seizures and decrease of consciousness. A CSF examination found a sign of infection and the working diagnosis is encephalitis.

Tasks:1. Brain tissue is protected from harmful microorganisms and hazardous materials by the Blood-

Brain Barrier, please explain the components of Blood-Brain Barrier and describe its microscopic structure.

2. Please explain the clinical importance of blood-brain barrier in the development of disease in the brain and its treatment.

Self Assessment 1. Explain the general structure of neuron!2. Mention and explain classification of neuron according to their structure and their function!3. Explain the Nisll’s Bodies!4. Mention the type and explain the function of neuroglial cells!5. Mention and explain various types of synapses between neuron!6. Brain consist of...................................and................................ 7. White matter is composed mostly by................., and Gray Matter is composed mostly

by......................8. Differentiate the histological structure between cerebrum and cerebellum9. Connective tissue that covered the brain and spinal cord is called by…………, its outermost

layer is…... intermediate layer is………., and the innermost layer is……….. 10. Blood-brain barrier is composed by.......11. Cerebro spinal fluid (CSF) is produced by..................12. Connective tissue which covers a nerve is....................., covers each bundle of nerve fiber

is................., and covers a nerve fiber is............13. Myelin sheath in CNS is produced by...............and in PNS by........14. Explain the classification of the nerves!15. Differentiate the structure of somatic and autonomic nervous system!16. Ganglia are..................., there are two types of ganglia :................and.............

NEUROPATHOLOGYDr. Ni Putu Sriwidyani, Sp.PA

ABSTRACTThe principal function unit of the central nervous system is the neuron. Of all the cells in the body, neurons have a unique ability to receive, store, and transmit information. Neurons of different types and in different locations have distinct properties, including functional roles, distributions of their connections, neurotransmitters used, metabolic requirements, and levels of electrical activity at a given moment. A set of neurons may thus show selective vulnerability to various insults because it shares one or more these properties.



The CNS is affected by a number of unique neurological disorders, and also responds to common insults in a manner that is distinct from other tissues.

LEARNING TASKCase 1A 30 year old women sees the Gynecologist because of amenorrhea since 1 year and infertility. On physical examination found galactorrhea and hemianopsia bitemporal.

Question:1. Elaborate sign and symptom of this patient with anamnesis and physical examination.2. Laboratory and imaging method should be performed3. What is the possible diagnosis of this tumor.

Case 2A 45 year old, previously healthy man has developed headaches over the past month. There are no remarkable findings on physical examination. A cerebral angiogram shows a 7 mm saccular aneurysm at the trifurcation of the right middle cerebral artery.Question:

1. What is the abnormal vascular disease found in this man?2. What is the complication of this abnormality

Case 3A 72 year old woman falls down the stairs. She does not lose consciousness. About 36 hours later, she develops a headache and confusion and is taken to the emergency department. On physical examination, she is conscious and has a scalp contusion on the occipital. What is the most likely location of an intracranial hemorrhage in this patient?

SELF ASSESMENTDescribe and give some example of:

1. Cerebral edema, hydrocephalus, and raised intracranial pressure. 2. Malformation and developmental disease3. Trauma affecting CNS4. Cerebrovascular disease5. CNS Infection6. Demyelinating disease7. Degenerative disease of CNS8. Tumors of CNS

DAY 7th

Clinical PathologyDr. dr. A.A. Ngurah Subawa, M.Si., SpPK

TOPIK : Cerebrospinal analysis

AIMS:To discribe the kind of CSF test how to interprete the test.

LEARNING OUTCOMES:



To discribe the interpretation of test.

CURRICULUM CONTENTS:a. Production of CSF.b. Spicemen collection.c. CSF examination and interpretation of test.

Abstract of the lecture:Lumbar puncture is frequently performed in primary care. Properly interpreted tests can make cerebrospinal fluid (CSF) a key tool in the diagnosis of a variety of diseases. Proper evaluation of CSF depends on knowing which tests to order, normal ranges for the patient’s age, and the test’s limitations. Protein level, opening pressure, and CSF-to-serum glucose ratio vary with age. Xanthochromia is most often caused by the presence of blood, but several other conditions should be considered. The presence of blood can be a reliable predictor of subarachnoid hemorrhage but takes several hours to develop. The three-tube method, commonly used to rule out a central nervous system hemorrhage after a “traumatic tap,” is not completely reliable. Red blood cells in CSF caused by a traumatic tap or a subarachnoid hemorrhage artificially increase the white blood cell count and protein level, thereby confounding the diagnosis. Diagnostic uncertainty can be decreased by using accepted corrective formulas. White blood cell differential may be misleading early in the course of meningitis, because more than 10 percent of cases with bacterial infection will have an initial lymphocytic predominance and viral meningitis may initially be dominated by neutrophils. Culture is the gold standard for determining the causative organism in meningitis. However, polymerase chain reaction is much faster and more sensitive in some circumstances. Latex agglutination, with high sensitivity but low specificity, may have a role in managing partially treated meningitis. To prove herpetic, cryptococcal, or tubercular infection, special staining techniques or collection methods may be required.

TRIGGER SCENARIO: A girl one years old taken by her father to emergency department with chief complained convulsion. Her father also complained about rhinitis, productive cough and fever since 5 days. LEARNING TASK:

1. Mention the kind of CSF test should be done!2. Described the location of CSF puncture in this patient!3. Mention the differential diagnosis of this patient!4. Mention the indication and contra indication of lumbal puncture!5. What are the CSF findings in bacterial meningitis? 6. What are the CSF findings in tuberculous meningitis?

SELF ASSESSMENT:1. How is CSF product ?2. What is the indication and contraindication of lumbar puncture ?3. How to normal value CSF analysis? 4. How to interprete the result of each test ?5. How to differentiate the red colour of CSF due to the artificial bleeding and the subarachnoidal

bleeding ?



6. Procedure collection of CSF?

PHARMACOLOGYDr. dr. I Made Jawi, M.Kes

DRUGS USED FOR SEIZURE DISORDERS AIMS :

1. Describe the rationale drugs used to treat each type of seizure2. Describe the desired therapeutics outcomes for seizure disorders3. Develop a education plan for people diagnosed with a seizure disorder

LEARNING OUTCOMES :Apply concepts and principles of drugs used for seizure

CURRICULUM CONTENT1. Basic pharmacology of anti seizure drugs

- Drugs used in partial seizures & generalized tonic-clonic seizures- Drugs used in generalized seizures- Other drugs used in management of epilepsy

2. Clinical pharmacology of anti seizure drugs- Management of epilepsy- Special aspect of the toxicology of anti seizure drugs

ABSTRACTSeizures are the result of the sudden, excessive firing of a small number of neurons and the

spread of electrical activity to adjacent neurons. There are several types and many causes of seizures. Identification of the cause of seizure activity is important in determining the type of therapy required. Contributing factors (e.g., head injury, fever, hypoglycemia, drug overdose) must be specifically treated to correct the underlying cause before chronic anticonvulsant therapy is started. Once the underlying cause is treated, it is rare that chronic antiepileptic therapy is needed. If the seizures are chronic and recurrent, the patient is diagnosed as having epilepsy. Epilepsy is treated almost exclusively with anticonvulsant medications. The goals of therapy are to reduce the frequency of seizure activity and minimize the adverse effects of the medicine. To attain this, therapy must be individualized to consider the type of seizure activity and the age, gender, and concurrent medical condition of the patient. Patients as well as their families require education and support regarding their responbilities in managing epilepsy.

SCENARIOMr X, 45 years old, suddenly had a tonic clonic seizure while attending a seminar. When his family notified of this and his need for transportation home, his wife tells you he has not been taking his medications regulary.

LEARNING TASK

1. Describe how you as a doctor would address this situation?2. Describe anti seizure drugs using in seizure patients?3. Describe adverse effect of anti seizure drugs using in seizure patients?



SELF ASSESMENT1. What is the definition of fetal hydantoin syndrome?2. Which one of antiseizure drugs can cause gingival hyperplasia?3. Can you describe the interaction of antiseizure drugs with the other drugs?4. What is the treatment of patient with status epilepticus?

PHARMACOLOGY MANAGEMENT OF PARKINSONISM & OTHER MOVEMENT DISORDERS

Dr. dr. I Made Jawi, M.Kes

AIMS :1. Describe the rationale drugs used to treat parkinson’s disease2. Describe the desired theraupetic outcomes for parkinson’s disease3. Develop a education plan for people diagnosed with parkinson’s disease

LEARNING OUTCOMES :1. Apply concepts and principles of drugs used for parkinson’s disease

CURRICULUM CONTENTDrug therapy for Parkinson’s Disease

- Drug class : Dopamine Agonists- Drug class : COMT Inhibitor- Drug class : Anti cholinergic Agents- Drug Class : Miscellaneous Anti parkinsonism Agents

ABSTRACTParkinson’s disease is a progressive neurologic disorder caused by deterioration of dopamine-

producing cells in the portion of the brain responsible for maintenance of posture and muscle tone and the regulation of voluntary smooth muscles. Normally a balance exists between dopamine, an inhibitory neurotransmitter, and acetylcholine, an excitatory neurotransmitter and acetylcholine, an excitatory neurotransmitter. The symptoms associated with Parkinson’s disease develop because of a relative excess of acetylcholine in the brain. The goal of treatment is to restore dopamine neurotransmitter function as close to normal as possible and relieve symptoms caused by “excessive” acetylcholine. Therapy must be individualized, but selegiline therapy is often started first to slow the development of symptoms. As selegiline becomes less effective, levodopa is started with or without selegiline. Dopamine agonists (amantadine, bromocriptine, pergolide, ropinirole, pramipexole) may be added to directly stimulate dopamine receptors. Entacapone may be added to levodopa therapy to reduce the metabolism of levodopa, prolonging its action. Anti cholinergic agents may be added at any time to reduce the effects of the excessive acetylcholine. Non pharmacologic treatment (e.g., diet, exercise, physical therapy) of Parkinson’s disease is equally important in maintaining the long-term well being of the patient.

SCENARIO



Mrs X, 55 years old, is being started on an anti cholinergic drug as part of the treatment plan for Parkinson’s disease.

LEARNING TASK1. What symptoms can be expected to improve?2. What problems could also arise from starting this medication?3. Discuss the normal course of progsession of Parkinson’s disease and include the rationale

for drug therapy to alleviate the symptoms4. List drugs which will give to the patient who has parkinsonism?5. Explain why do you choose l-dopa and not dopamine to treat Parkinson’s disease?6. Explain why levo-dopa could not be combined with pyridoxine?7. Describe the benefit combination of levodopa with carbidopa in the treatment of

Parkinsonism?8. Describe why dipenhydramine used to treat Parkinsonism caused by neuroleptic?

SELF ASSESMENT1. Describe the rationale drugs used to treat parkinson’s disease2. Describe the side effect of drugs that used for parkinson’s diseas3. Develop an education plan for people diagnosed with parkinson’s disease

TOPIK STUDENT PROJECT

Regular Class (Class A)GroupSGD Judul Student project Pembimbing Evaluator

1 BPPV Facilitator dr. Kt. Widiastuti, Sp.S2 Lesi Batang Otak Facilitator dr. Kt. Widiastuti, Sp.S3 Duchene muscular dystrophy Facilitator Dr. Dr. Anna Marita,Sp. S(K)4 Cerebral Palsy Facilitator Dr.dr. Anna Marita, Sp.S (K)5 Temporal giant arteritis Facilitator dr. Md. Oka Adnyana, Sp.S (K)6 Red Falg cephalgia Facilitator dr. Md Oka Adnyana, Sp.S(K)7 CT scan Otak dan interpretasi Facilitator dr. Made Widhiasih, Sp. Rad8 Neurogenic bladder Facilitator Dr. Kumara Tini, Sp.S , FINS9 Amyotrophic Laterosclerosis Facilitator Dr. dr.Thomas Eko, Sp.S (K)10 Mild Cognitive Impairment Facilitator Dr. dr. AAA Putri Laksmidewi, Sp.S (K)

English Class (Class B)GroupSGD Judul Student project PEMBIMBING EVALUATOR

1 Afasia Facilitator dr. Kt Widiastuti, SP.S2 Chorea dan dystonia Facilitator Dr.dr. DPG. Purwa Samatra, Sp.S (K)3 Essential tremor Facilitator Dr. Dr. DPG. Purwa Samatra, Sp.S(K)

4 Cranio-cerebral Congetinal defect Facilitator Prof. Dr.dr. Sri Maliawan,SP.BS

5 Cauda Equina SYndrome Facilitator Dr.dr. Tjokorda Gde Mahadewa, Sp.BS(K) Spinal



6 Toxoplasmosis cerebri Facilitator Dr. Susilwathi, Sp.S7 Syringomyelia Facilitator Dr.dr. Made Golden, Sp.BS (K)8 Myelopathy Facilitator Dr. AABN, Nuartha, Sp.S (K)9 Neurocysticercosis Facilitator Prof. Dr.dr. Raka Sudewi, Sp.S (K)

10 Horner syndrome Facilitator Dr. IA Sri wijayanti



Clinical Neuroscience Semester IVTopic and Schedule English Class

Date Topic/Module Class B Venues Conveyer1

May 26th

2016

Student project

Vertigo, Bell’s palsyand Meniere Disease

Hearing loss and Tinnitus

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Ketut Widiastuti Sp.S

dr. Made Wiranadha Sp.THTKL

Facilitators.

dr. Ketut Widiastuti , Sp.Sdr. Made Wiranadha Sp.THTKL

2May 27th

2016

Student project

Kejang Demam (pediatric)

Seizure, Epilepsy and Status Epilepticus

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Dewi Sutriani Maharini, Sp.A

Dr. dr. Anna Marita, Sp.S(K)

Facilitators.

dr. Dewi Sutriani Maharini, Sp.A/ Dr.dr. Anna Marita, Sp.S(K).



3May 30th

2016

Student project

Tension Headache and Cluster

Imaging interpretasi x-Ray tengkorak dan tulang belakang

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Made Oka Adnyana, Sp.S(K)dr. Made Widhiasih, SpRad

Facilitators.

dr. Made Oka Adnyana, Sp.S(K)/dr. Made Widhiasih, SpRad

4May 31st

2016

Student project

Migren and Neuralgia Trigeminal

Imaging

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00 10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00 15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Made Oka Adnyana, Sp.S(K)

dr.Made Widhi Asih, SpRad

Facilitators.

dr. Made Oka Adnyana, Sp.S(K)/dr.Made Widhi Asih, SpRad

5June 1st

2016

Student project

HNP, Radicular syndrome

Acute and refered pain

Surgical aspect of disc herniation

SGD

Plenary

09.00-11.00 11.00-12.00

12.00-13.00

13.00-14.00

14.00-15.00 15.00-16.00

Class room

Class room

Class room

Disc. Room

Class room

dr. IA Sri Wijayanthi, Sp.S

Dr. dr. Pt. Pramana, Sp.AN., M.Kes.

Dr.dr. Tjok Mahadewa, Sp.BS(K) spinal

Facilitators.

dr. IA Sri Wijayanthi, Sp.S, BiomedDr. dr. Pt. Pramana, Sp. An.,M.Kes. Dr.dr. Tjok Mahadewa,



Sp.BS(K) spinal6

June 2nd

2016

Student project

CTS, TTS, peroneal palsy

Neuropathic pain, neuropati, HNP

Surgical aspect of peripheral nerve lesion

SGD

Plenary

09.00-11.00

11.00-12.00

12.00-13.00

13.00-14.00

14.00-15.00

15.00-16.00

Class room

Class room

Class room

Class room

dr. IA Sri Wijayanthi Sp.S, Biomed Sp.S

dr. IA Sri Wijayanthi Sp.S, Biomed Sp.S

Dr.dr.Tjok Mahadewa, Sp.BS (K) spinal

Facilitators

dr. IA Sri Wijayanthi Sp.S, Biomed Sp.S/ Dr.dr.Tjok Mahadewa, Sp.BS (K) spinal

7June 3rd

2016

Student project

Dementia/ Alzheimer/ Amnesia pasca trauma

Movement Disorder/Neurogeriatric

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Widiasttuti, Sp.S

Dr.dr. DPG. Purwa Samatra, Sp.S(K)

Facilitators.

dr. Widiasttuti, Sp.S/ Dr.dr. DPG. Purwa Samatra, Sp.S(K)

8June 6th

2016

Student project

CNS Tumor primer dan sekunder

Traumatic Brain Injury, hematom epidural, hematom subdural.

Neurofuncional

09.00-11.00 11.00-12.00

12.00-13.00

13.00-14.00

Class room

Class room

Class room

dr. Susilawathi, Sp.S

Prof. Dr. dr. Sri Maliawan, SpBS(K)

Prof. Dr. dr. Sri Maliawan,



surgery

SGD

Plenary

14.00-15.00

15.00-16.00

Disc. room

Class room

SpBS(K)

Facilitators.

dr. IA. Sri Wijayanti, Sp.S/ Prof. Dr. dr. Sri Maliawan, SpBS(K)

9June 7th

2016

Student project

TIA, Infark cerebral, hematoma intraserebral, SAH

Stroke 2 (management )

Stroke 3 (surgical management)

SGD

Plenary

09.00-11.00 11.00-12.00

12.00-13.00

13.00-14.00

14.00-15.00

15.00-16.00

Class room

Class room

Class room

Disc. room

Class room

dr. Kumara Tini, Sp.S , FINS

dr. Kumara Tini, Sp.S , FINS

dr. Wayan Niryana, M.Kes, SpBS(K)

Facilitators.

dr. Kumara Tini, Sp.S , FINS/ dr. Wayan Niryana, M.Kes, SpBS (K)

10June 8 th

2016

Student project

Trauma Medula spinalis, Complete spinal transection, acute medulla compression

Surgical aspect of brain tumors

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc. room

Class room

Dr.dr. Tjokorda GB. Mahadewa, M.Kes., SpBS(K)Spinal

Dr.dr. Made Golden , Sp.BS (K)

Facilitators.

Dr.dr. TjokordaGB. Mahadewa, M.Kes.,SpBS(K)Spinal/ Dr.dr. Made Golden Sp.BS(K)

11June 9th

Student Project 09.00-10.00



2016 GBS, Myastenia Grafis

Ensefalopati, Koma

BreakIL/Self Ass

SGD

Plenary

10.00-11.00

11.00-12.00

12.00-12.3012.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc room

Class room

Prof. Dr.dr. Raka Sudewi, Sp.S (K), SP.S

dr. Kumara Tini, Sp.S, FINS

Facilitators.

Prof. Dr.dr. Raka Sudewi, Sp.S (K)/ dr. Kumara Tini, Sp.S, FINS

12June 10th

2016

Student project

Meningitis, ensefalitis, malaria serebral, Rabies

CNS HIV/AIDS, Poliomielitis, tetanus, tetanus neonatorum

Break.

IL/Self Ass.

SGD

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-13.30

13.30-15.00

15.00-16.00

Class room

Class room

Disc room

Class room

Prof. Dr. dr. Raka Sudewi,Sp.S(K)

Prof. Dr. dr. Raka Sudewi,Sp.S(K)

Facilitators.

Prof. Dr. dr. Raka Sudewi,Sp.S(K)Day/Date Activity Class B Venue ConveyorJune 13th

2016

June 14th

2016

June 15th

2016

June 16th

2016

June 17th

Presentasi Student project

Basic clinical skillMotorik, koordinasi, sensorik

Basic clinical skillFungsi luhur dan refleks

Basic clinical skillFungsi saraf kranial, Tulang belakang dan meningeal sign, tanda ischialgia

Basic clinical skill

10.00-12.00

11.00-13.00

11.00-13.00

11.00-13.00

11.00-13.00

Ruang sidang lt.IV

Skill Lab

Skill Lab

Skill Lab

Skill Lab

Semua Lecturer

dr. I.A Sri Wijayanti, M.Biomed, Sp.S

dr. Ketut Widyastuti, Sp.S

dr. Ni Made Susilawathi, Sp.S




2016 Pemeriksaan DiagnostikRadiologi dan elektrodiagnostik

June 20th

2016 EVALUATION 08.30-10.30

Clinical Neuroscience Semester IV

Topic and Schedule Regular ClassDate Topic/Module Class A Venues Conveyer

1May 26th

2016

Vertigo, Bell’s palsyand Meniere Disease

Hearing loss and Tinnitus

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. Room

Class room

dr. Ketut Widiastuti Sp.S

dr. Made Wiranadha Sp.THTKL

Facilitators.

dr. Ketut Widiastuti , Sp.Sdr. Made Wiranadha Sp.THTKL

2May 27th

2016

Kejang Demam (pediatric)

Seizure, Epilepsy and Status Epilepticus

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. Room

Class room

dr. Dewi Sutriani Maharini, Sp.A

Dr. dr. Anna Marita, Sp.S(K)

Facilitators.

dr. Dewi Sutriani Maharini, Sp.A/Dr.dr. Anna Marita, Sp.S(K).

3

May 30th

Tension Headache and Cluster Headache

08.00-09.00 Class room dr. Made Oka Adnyana, Sp.S(K)



2016 Imaging interpretasi x-Ray tengkorak dan tulang belakang

IL/Self Ass.

SGD

Break.

Student project

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Disc. Room

Class room

dr. Made Widhiasih, SpRad

Facilitators.

dr. Made Oka Adnyana, Sp.S(K)/dr. Made Widhiasih, SpRad

4May 31st

2016

Migren and Neuralgia Trigeminal

Imaging

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. Room

Class room

dr. Made Oka Adnyana, Sp.S(K)

dr.Made Widhi Asih, SpRad

Facilitators.

dr. Made Oka Adnyana, Sp.S(K)/dr.Made Widhi Asih, SpRad

5June 1st

2016

HNP, Radicular syndrome Acute and refered pain

Surgical Aspect of Disc Herniation

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Class room

Disc. Room

Class room

dr. Komang Arimbawa, Sp.S

Dr. dr. Pt. Pramana, Sp.AN., M.Kes.

Dr.dr. Tjok Mahadewa, Sp.BS (K) Spinal

Facilitators.

dr. Dr. Komang Arimbawa, Dr. dr. Pt. Pramana, Sp.AN.,M.Kes.Dr.dr. Tjok Mahadewa, Sp.BS (K) Spinal

6June 2nd

2016

CTS, TTS, peroneal palsy

08.00-09.00 Class room Dr. dr. Thomas Eko ,Sp.S(K), FAAN



Neuropathic pain, neuropati, HNP

Surgical aspect of peripheral nerve lesion

SGD

Break.

Student project

Plenary

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. Room

Class room

Dr. dr. Thomas Eko ,Sp.S(K), FAAN

Dr.dr. Tjok Mahadewa, Sp.BS (K) Spinal

Facilitators.

Dr. dr. Thomas Eko ,Sp.S(K), FAAN/ Dr.dr. Tjok Mahadewa, Sp.BS (K) Spinal

7June 3rd

2016

Dementia/Alzheimer/Amnesia pasca trauma

Movement Disorder/Neurogeriatric

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. Room

Class room

Dr.dr. AAA Putri Laksmidewi, Sp.S (K)

Dr.dr. DPG. Purwa Samatra, Sp.S(K)

Facilitators.

Dr.dr. AAA Putri Laksmidewi, Sp.S (K)/Dr.dr. DPG. Purwa Samatra, Sp.S(K)

8June 6th

2016

CNS Tumor primer dan sekunder

Traumatic Brain Injury, hematom epidural, hematom subdural.Neurofunctional Surgery

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Class room

Disc. room

Class room




Facilitators.

dr. Susilawathi, Sp.S/ Prof. Dr. dr. Sri Maliawan, SpBS(K)



9June 7th

2016

TIA, Infark cerebral, hematoma intraserebral, SAH

Stroke 2 (management)

Stroke 3 (surgical management)

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Class room

Disc. room

Class room

dr. AABN.Nuartha, Sp.S(K)

dr. AABN.Nuartha, Sp.S(K)

dr. Wayan Niryana, M.Kes, SpBS(K)

Facilitators.

dr. AABN.Nuartha,Sp.S(K)/ dr. Wayan Niryana, M.Kes, SpBS (K)

10June 8 th

2016

Trauma Medula spinalis, Complete spinal transection, acute medulla compression

Surgical aspect of brain tumors

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc. room

Class room

Dr.dr. Tjokorda Mahadewa, M.Kes., SpBS(K)Spinal

Dr.dr. Made Golden, Sp.BS (K)

Facilitators.

Dr.dr. Tjokorda . Mahadewa, M.Kes., SpBS(K)Spinal / Dr.dr. Made Golden SP.BS(K)

11June 9th

2016

GBS, Myastenia Grafis

Ensefalopati, Koma

IL/Self Ass.

SGD

Break.

Student project

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

Class room

Class room

Disc room

dr. Susilawathi, SP.S


Facilitators.

dr. Susilawathi, Sp.S/



Plenary 14.00-15.00 Class room dr. Kumara Tini, Sp.S, FINS12

June 10th

2016

Meningitis, ensefalitis, malaria serebral, Rabies

CNS HIV/AIDS, Poliomielitis, tetanus, tetanus neonatorum

IL/Self Ass.

SGD

Break.

Student project

Plenary

08.00-09.00

09.00-10.00

10.00-11.00

11.00-12.00

12.00-12.30

12.30-14.00

14.00-15.00

Class room

Class room

Disc room

Class room



Facilitators.

dr. Susilawathi, Sp.SJune 13th

2016

June 14th

2016

June 15th

2016

June 16th

2016

June 17th

2016

Presentasi Student project

Basic clinical skillMotorik, koordinasi, sensorik

Basic clinical skillFungsi luhur dan refleks

Basic clinical skillFungsi saraf kranial, Tulang belakang dan meningeal sign, tanda ischialgia

Basic clinical skillPemeriksaan DiagnostikRadiologi dan elektrodiagnostik

08.00-10.00

08.00-11.00

08.00-11.00

08.00-11.00

08.00-11.00

Ruang sidang lt.IV

Skill Lab

Skill Lab

Skill Lab

Skill Lab

Semua Lecturer

dr. I.A Sri Wijayanti, M.Biomed, Sp.S


dr. Ni Made Susilawathi, Sp.S


June 20th

2016 EVALUATION 08.30-10.30



LEARNING PROGRAM CLINICAL NEUROSCIENCEDAY 1st

May 26th2016.VERTIGO, MENIERE DISEASE AND BELL’S PALSY


Aims:Describe diagnosis, initial management and/ or referral patients with vertigo

Learning outcome:Can describe the:

1. Type of dizziness2. Differentiation between peripheral vestibular vertigo and central vestibular vertigo3. Differentiation between vestibular vertigo and non vestibular vertigo4. Examinations of dizzy patients5. Initial management principle for vertigo6. Evaluation the need for urgent investigations and referrals

Curriculum contens:1. History taking of Dizziness2. Physical Examination of dizzy patients3. Investigation routine and specific of vertigo4. Initial Management for vertigo

AbstractsVertigo is an unpleasant disturbance of spatial orientation or illusory perception of movement of the body (spinning and wobbing) and/or of the surrounding that usually results in a disturbance of equilibrium system.The sense of balance (the equilibrium system) is provided by integration of inputs from the visual, proprioceptive, and vestibular system into the brain. Pathologies along these pathways results in dizziness with various forms and severity.Dizziness as general term, can be subdivided into vertigo, disequilibrium, dizziness and presyncope. The patients whose dizziness is considered vertiginous, the evaluation should be directed toward differentiating between peripheral and central pathology

Self directing learningBasic knowledge that must be known:

1. The Equilibrium System and The Vestibular System2. Peripheral vestibular vertigo3. Central vestibular vertigo4. Non vestibular vertigo

ScenarioA 38-year old- man rolled over in the bed early morning and suddenly developed severe

nausea as well as the unpleasant sensation that room was spinning around him. The spinning resolved within 30 seconds but recurred again in the opposite direction when he rolled back to his original



position. This had never happened to him before. The patient denied tinnitus, hearing loss, recent viral illness and head trauma.

Learning Task:1. From the history above, what need to be asking to the patient ?

(remember the secret seven and fundamental four)2. Make the physical examination of patient with imagination in correlation with the story above !3. How to differentiate between patient with peripheral and central vestibular vertigo?4. How to differentiate between vestibular vertigo and non vestibular vertigo?5. What is the differential diagnosis of this patient?6. Please explain the pathogenesis from each of differential diagnosis that has been mention

above!7. What is the initial management of this patient ?

Self Assessment 1. How to do a good history taking in vertigo cases? 2. How to do a good physical examination in vertigo cases?3. What is the etiology of peripheral and central vertigo?4. What is the pathogenesis of Benign Paroxysmal Positional Vertigo(BPPV) and Meniere’s

disease?5. When do you refer the patient with vertigo?

MENIERE

Aims:Describe diagnosis, initial management and/ or referral patients with meniere disease


1. Diagnosis of meniere disease2. Differential Diagnosis of meniere disease3. Management for meniere disease4. Prognosis of meniere disease5. Further investigations and referrals

Curriculum contens:1. History taking of meniere disease2. Physical Examination of meniere disease3. Investigation routine and specific of meniere disease4. Management for meniere disease

AbstractsMeniere disease also called endolymphatic hydrops, is a disorder that can affect hearing and balance to a varying degree. Meniere disease is chronic disorder in inner ear, it’s not fatal but disturb the quality of life. It is characterized by episodes of vertigo, low-pitched tinnitus, and hearing loss. The hearing



loss is fluctuating rather than permanent, meaning that it comes and goes, alternating between ears for sometime, then becomes permanent with no return to normal function. It is named after the French physician Prosper Meniere, who, in an article published in 1861, first reported that vertigo was caused by inner ear disorders. The condition affects people differently; it can range in intensity from being a mild annoyance to a lifelong condition. Meniere often begins with one symptom, and gradually progresses. However, not all symptoms must be present to confirm the diagnosis although several symptoms at once is more conclusive than different symptoms at separate times. The symptoms of Meniere are variable; not all sufferers experience the same symptoms. According guidelines of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), Meniere disease have four symptoms:

1. Attacks of rotational vertigo that can be mild to severe, unpredictable, and minimal 20 minutes for 1 episode, but generally no longer than 24 hours.

2. Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss, usually in lower frequencies. Getting worsen during attack.

3. Unilateral or bilateral tinnitus, with characteristic low frequency or roaring noise.4. A sensation of fullness or pressure in one or both ears.

Some may have parasympathetic symptoms, which aren't necessarily symptoms of Meniere, but rather side effects from other symptoms. These are typically nausea, vomiting, and sweating which are typically symptoms of vertigo, and not of Meniere. Vertigo may induce nystagmus, or uncontrollable rhythmical and jerky eye movements, usually in the horizontal plane, reflecting the essential role of non-visual balance in coordinating eye movements..

ScenarioA 38-year old- woman come to a clinic with chief complaint vertigo with mild symptoms, then

progress to severe from this morning. She also hear roaring noise and fullness in her ears, and there also hearing loss that more severe in right ear. One week before the symptoms appear, she feel tired and eat much salty food.

Learning task:1. From the history above, what need to be asking to the patient ?

(remember the secret seven and fundamental four)2. Make the physical examination of patient with imagination in correlation with the story above !3. What is the differential diagnosis of this patient?4. Where is topical lesion on this case? 5. How to differentiate between Meniere and BPPV patient?6. Please explain the pathogenesis from each of differential diagnosis that has been mention

above!7. What is the management of this patient ?8. When do we start to rehabilitate the patient ?

BELL’S PALSYAims:Describe diagnosis, management and/ or referral patients with facial palsy


1. Diagnosis of Bell’s Palsy



2. Differential Diagnosis of Bell’s Palsy3. Management for Bell’s Palsy4. Prognosis of Bell’s Palsy5. Further investigations and referrals

Curriculum contens:1. History taking of Bell’s Palsy2. Physical Examination of facial palsy patients3. Investigation routine and specific of Bell’s Palsy4. Management for Bell’s Palsy

AbstractsBell’s Palsy is clinical syndrome of idiopathic acute unilateral facial paralysis. Patients may

report the exposure to cold preceded their symptoms. The face often described as feeling stiff and numb without any objective sensory deficit. Decrease tearing and hyperacusis may appear in some cases may precede weakness.The condition is thought to be related to a viral infection, the swollen nerve being entrapment in the facial canal. Although not life threatening, Bell’sPalsy may have severe functional, aesthetic, and psychological consequences.

Self directing learningBasic knowledge that must be known:

1. The anatomy of Facial nerve2. Facial Palsy3. Bell’s Palsy4. Factors that affect Bell’s Palsy

ScenarioA 24-year old- medical student noticed while shaving one morning that he was unable to move

the left side of his face. He worried that a serious problem, possibly a stroke, might be have occurred. He had had influenza-like symptoms the week before this sudden attack.Learning task:

1. From the history above, what need to be asking to the patient ?(remember the secret seven and fundamental four)

2. Make the physical examination of patient with imagination in correlation with the story above !3. What is the differential diagnosis of this patient?4. Where is lesion base on facial nerve pathway (make topical diagnosis)? 5. How to differentiate between facial palsy in Bell’s Palsy and Stroke patient?6. Please explain the pathogenesis from each of differential diagnosis that has been mention

above!7. What is the management of this patient ?8. When do we start to rehabilitate the patient ?

Self assessment1. How to do a good history taking in Facial Palsy cases? 2. How to do a good physical examination in Facial Palsy cases?3. When do you refer the patient with Facial Palsy?

Refferences:



1. PERDOSSI. Pedoman dan Tatalaksana Vertigo 20122. Adam and Victor’s. Principles of Neurology 8th.3. Wikipedia. Meniere Disease

HEARING LOSSdr. Made Wiranadha, Sp. THT-KL

AbstractThere are two major categories of hearing loss that are key concepts for the clinician to understand. The first, conductive hearing loss, is due to an outer or middle ear problem—a problem “conducting” sound waves through the ear canal to the eardrum and then through the middle ear apparatus toward the inner ear. Causes of conductive loss might include obstruction of the ear canal by cerumen (wax), impairment of middle ear function by fluid, or fixation of the middle ear ossicles by disease. With conductive loss, sounds coming from within, such as one’s own voice, are perceived as louder because of reduced competing ambient noise. Plug your right ear with your finger, creating a conductive loss, and note how your own voice sounds louder on this side. This phenomenon is known as autophony. A patient with a conductive loss often feels like he or she is talking “in a barrel,” or “under water.”

Sensorineural hearing loss is due to a malfunction somewhere in the inner ear, from the cochlea inward through the auditory nerve. This is often termed “nerve deafness” and with this type of loss even one’s own voice does not sound loud. The distinction between these two types of loss is obviously important for determining the cause of a patient’s hearing complaint. Both conductive and sensorineural loss in the same ear. This would be referred to as a mixed loss. Tuning-fork evaluation can differentiate between the two hearing loss. The 512-Hz tuning fork is themost accepted frequency for assessing hearing using the Weber and Rinne tests. Audiometry is the precise method of hearing assessmentLearning Objective

1. Describe general strategy in the approach to patients with hearing loss a trough history and physical examination supported by selected and supporting tests or special technique investigations.

2. Describe etiopathogenesis and pathophysiology of hearing loss with it’s clinical implication such as congenital hearing loss, hearing loss due to trauma, hearing loss due to an infection, and others.

3. Implement the differential diagnosis of congenital hearing loss, trauma or aging.4. refer patient with hearing loss cases that can be treated eg sudden deafness.

Learning ObjectiveCASE 1A 19 years woman complained of impaired hearing in the right ear suddenly after swimming, the ear feels full, and pain. Patients do not complain of cough and colds.

Learning Task1. What question is needed to complete anamnesis?2. Describe etiology and pathophysiology of this hearing loss?3. Describe about diagnose of the disease and learn symptoms and sign, plan of the treatment and

complication could be of the disease?

Case 2



A 3 years old boy was brought to the ENT-HNS clinic with complaints has not been able to speak to the present, the patient does not respond when called upon. The patient does not respond well to hear the sound of thunder or a loud closed door.

Learning Task 1. What question is needed to complete anamnesis? 2. What investigations are needed?3. Describe about plan of the treatment of the disease?

FromMenner, A Pocket Guide to the Ear © 2003 Thieme

DAY 2nd

May 27th 2016FEBRILE SEIZURE IN CHILDRENdr. Dewi Sutriani Mahalini, Sp.A

Aims:Describes definition, pathophysiology, classification and consensus/guideline management of febrile seizures. Learning outcome:

1. Describe definition and classification of febrile seizure in children.2. Describe etiology and risk factors of febrile seizure in children.3. Describe the sign, symptom and diagnosis criteria of febrile seizure in children.4. Describe the management febrile seizure and long term management for prevention recurrent

seizure.5. Describe the necessary information and education for parents and social environment.

Curriculum contents:1. Consensus of diagnosis and management febrile seizure 2. Classification of febrile seizure3. Risk factors of recurrent febrile seizure and genetic epilepsy with febrile seizures plus (GEFS+)4. Immediate medical management of acute seizure and status epilepticus5. Long term management for prevention of recurrent febrile seizure (intermittent and long term

prophylaxis)

Abstract of LectureFebrile seizures (FS) are the most common seizure disorder in childhood. Seizures with fever

occur in 3- 5% of children in North America and Europe, and in up to 14% of children IN Asia. It affects both boys and girls equally, mainly between 6 and 36 months with a peak at an age of 18 months. A febrile seizure (FS) is a disorder that presents between 3 months and 6 years of age with convulsions and fever but without evidence of intracranial infection or defined cause. It is defined as a seizure occurring in the context of a febrile illness, not secondary to a central nervous system (CNS) infection or an altered metabolic state in children who have not had neonatal or previous afebrile seizures.

There are two main clinical forms: Simple febrile seizure are a short generalized seizure, of a duration lasting than 15 minutes,not recurring within 24 hours, occurring during a febrile episode, not caused by an acute disease of the nervous system. Simple febrile seizures usually occurring during the



first 24 hours of a febrile illness. Majority (70-75%) of FS are simple febrile seizure. Complex febrile seizure are a focal, or generalized and prolonged seizure, of a duration of greater than 15 minutes, recurring more than once in 24 hours, and/or associated with post-ictal neurologic abnormalities, more frequently a post ictal palsy (Todd’s palsy), or with previous neurologic deficits (American Academy of Pediatrics 1996; Berg & Shinnar, 1996; Knudsen, 2000).

Risk of further febrile seizures: Approximately 30-40% of children who have a febrile seizure will have a recurrence, usually within 12 months. A higher risk of recurrence exists if the first seizure occurs when the patient is younger than 15 months, there is a history of febrile seizure in a first-degree. The majority are simple febrile seizures and therefore last a shorter duration and may abort spontaneously. The risk factors for developing febrile seizures are multiple and include both genetic factors such as positive family history of FS and environmental factors such as day care attendance, specific infections such as human herpes virus 614, influenza A virus15 and metapneumovirus16, prolonged stay in a neonatal unit, neuronal abnormality and iron deficiency anaemia.

The etiology of FS is considered to multifactorial model; however, an autosomal dominant inheritance with reduced penetrance has been described in several families. Several chromosomal loci, particularly those on 19q and chromosome 2, have been identified. Gene mutations on voltage gated ion channels such as the alpha 1 subunit, the alpha 2 subunit and beta 1 subunit of sodium channel (SCN1A , SCN2A and SCN1B) and those affecting the gamma amino butyric acid (GABA) receptor have been shown to be strongly associated with the epilepsy syndrome of ‘genetic epilepsy with febrile seizures plus’ (GEFS+).

Although a change in body temperature is required for occurrence of FS, the convulsions are not specifically related to the rise in temperature or height of the temperature. They are considered to be due to increased neuronal excitability due to release of various pyrogens.

Diagnosis is essentially based on physical examination and history taking (American Academy of Pediatrics, 1996). The initial evaluation includes exclusion of infection in the CNS.

Immediate medical management includes treatment of the seizure if still continuing. Benzodiazepines administered rectally, buccally or nasally are useful for rapid control. Since most FS are simple and abort spontaneously the use of intermittent or long term prophylaxis is not recommended. Diazepam over the first 24- 48 hours of each febrile illness has been in use since 1978 for intermittent prophylaxis; however its efficacy in the meta-analysis is controversial. In children with very frequent atypical febrile seizures, particularly those with recurrent prolonged seizures, long term treatment with sodium valproate may be beneficial.

ScenariosCase 1

A girl, 12 months of age, came to the emergency unit with main complaint seizure. Seizure occur once at 2 hours before admission, the tipe of seizure were tonic clonic, general, both eyes looking upward, the duration 10 minutes and stopped spontaneously. She look weak after seizure and next cried loudly after 15 minutes. The physical examination revealed, alert, respiration 28 times/minutes, pulse 100 times/minutes, rectal temperature 39.5oC. She also had cough, running nose.The urination was clear and yellow, but the patient had vomiting about 5 times and diarrhea 4 times since 2 days before admission.

Learning task1. What is the diagnosis and differential diagnosis? Explains the reason of your answers?2. What are the risk factor that you have to know?3. Explain possible causes of the acute seizure?4. What are the necessary diagnosis work up to support your diagnosis?



5. What are the management at emergency unit? 6. Should the patient hospitalized? Explain the reasons of your answer!7. Explain long term management to the patient!8. What are information and education that should be you done?

Case 2A boy, 4 years of age, came to the emergency unit with main complaint serial seizure. The first seizure occur 4 hours before admission, second seizure occur since 15 minutes ago and the seizure still continued until the patient arrive at emergency unit and still continued after treatment with diazepam rectally. Tipe of seizure were tonic clonic, general, both eyes looking upward. She look weak after seizure and still unconscious. The past history : patient already had seizure 3 times episode since 12 months of age, History of delivery were spontaneous, body weight 2000 grams and severe asphyxia. The physical examination revealed, respiration 30 times/minutes, pulse 120 times/minutes, rectal temperature 40.0oC. She also had history of cough and difficult breathing since 2 days before admission. The urination was clear and yellow, defecation normal.

Learning task1. What is the diagnosis and differential diagnosis? Explains the reason of your answers?2. What are the risk factor of recurrent seizure in this patient? 3. What are past history of seizure that you need to know for long term management?4. Explain possible causes or etiology of the acute seizure?5. What are the necessary diagnosis work up to support your diagnosis?6. What are the management for acute seizure? 7. Explain long term management to the patient!8. What are information and education that should be you done?

Self assessment1. Describe definition of febrile seizure in children!2. Describe classification of febrile seizure in children and its differentiation!3. Describe etiology and risk factors of febrile seizure in children!4. Describe the management of acute seizure in febrile seizure!5. Describe the long term management for prevention recurrent seizure!

EPILEPSY AND STATUSEPILEPTICUSDr. dr. Anna Marita Sinardja, Sp.S(K):

Aims:Describe pathophysiology, diagnosis, early manage and referral patien with seizuresLearning Outcome :

1. Describe the role of neurotransmitters on patophysiology of seizures2. Describe the neurological sign and symptom of seizures.3. Describe the classification of epilepsy4. Describe the Electroencephalography to diagnose epilepsy.5. Describe early manage the patiens with seizures and know indication dan adverse

effect of anti epileptic drugs (AEDs),



Curriculum Contens :1. Anatomy of cerebral cortex and hypocampus.2. Role of neurotransmitters3. Classification of epilepsy and seizures type.4. Etiology of epilepsy5. Role of Anti Epileptic Drugs (AEDs)6. Adverse effect of AEDs7. Psychosocial aspect of epileptic patiens

Abstract of Lectures.Epilepsy is defined as a condition in which to prone epileptic seizures. Epilepsy is recurrent of convulsion and stereotype. An epileptic seizures is caused by a trancient, excessive and abnormal discharge of nerve cells. The abnormal discharges my involve a small part of the brain or a much more extensive area in a both hemispheres. Epilepsy may be classified according to: seizurestype, EEG finding, aetiology, anatomical finding and age. International league Agants Epilepsy had a concensus to classified epileptic seizures as a:

A. Partial epilepsy : simple partial . partial complex and partial become generalB. General seizure : absence , tonic-clonic, clonic, tonic.C. Non classified

]

Pathophysiology of seizures is underlying of abnormality between inhibition and excitatory neurotransmitters. Less of inhibition or over of excytatory neurotransmitter may be causes. In the figure less of inhibitory neurotransmitter (GABA gamma amino butyric acid ) and over of the excitatory neurotransmitters (Glutamate) may be causes of the seizures.

Common causes of epileptic seizures are listed: A. Idiophatic/cryptogenic (unknown causes).B. Cerebral infections .C. Head trauma (traffic accident).D. Cerebrovascullar disease,E. Congenital disorders,.F. Metabolic disorders (renal, hepatic, hematological).G. Disorder during pregnance.H. Disorder during labour.

Diagnosis of epilepsy is essentially by a clinical features. Although investigation as EEG, Brain-scan and MRI may provide assistance. The diagnosis of epilepsy is made largely on the basis of the clinical history.



The drug treatment of epileptic patients has improved over recent years. There is much understanding of the principles of effective drug treatment with Anti Epileptic Drugs (AED). Practice point to manage patient with epilepsy is : Drugs treatment should be instituted only if the diagnosis of epilepsy is firm. Monotheray should be the role in the initial treatment of epilepsy and all drugs should be stated at low dosage, and built up over a period of weeks.

Treatment of epilepsy is long life. The treatment will be stop if the patiens have two years seizures free and EEG within normal limit. Psycososial problem in epileptic patiens shoul be manage because many patient with epilepsy have a psycososial problem.

Trigger/Scenario.

Case 1 (day 1)A 20-year-old women has history automobile accident 5 years ago, and has a decreas of the consciousness 30 minute after accident. 3 days before she go to hospital she has general convulsion and a automatism movement like a behavior changes.Neurological examination, no neurological deficit, physical examination within normal limit.

Learning task 1. What is the diagnosis?2. Explain why the traffic accident become to convulsion?3. What is the diagnosis tool you made to definite diagnosis?

Self assessment1. Describe the function of neurotransmitters.2. Describe the type of accident will become a seizures.3. Describe the classification of epilepsy, in the patiens like this case.4. Describe the diagnosis tool, in patiens whit seizures.

Disscusion in groupsWhere the TOPICAL DIAGNOSIS in patient with :

1. Hemiplegia on right side.2. Monoplegia superior extremity on left side3. Hemiplegia alternans N III on left side4. Tetraplegia5. Paraplegia.

Case 2 (day 2)Pregnacy women 25 years old, has a convulsion 3 days before she come to neurologic ward. The conculsion is generalized type. Physical examination within normal limit. No deficit neurology.Learning task

1. What is the diagnosis of the patiens?2. Why the pregnancy can induced seizures/convulsion?3. What kind of the drugs you can give to the patiens?



Case 3 (day 2)As a doctor who work in health-centre, you care the patienswith convulsion and after convultion the patiens had neurological deficit as a hemipharesis on right side and disappear before 24 hours.

Learning task1. When you conclusion hemipharesis in this patients ?2. How you differential diagnosed hemipharesis doe to organic lesion in the brain ? Where the

topical diagnosis the patients with hemipharesis on right side ?3. How to manage the patients who had hemipharesis after seizures ?

Self assessment1. Describe the epileptic patients with hemipharesis ?2. Describe the epileptic patiens with psyco-social handicap.3. Describe the manage patients with seizures and hemipharesis.

DAY 3rd and 4th

June 30th & 31st 2016HEADACHE (TENSION TYPE HEADACHE, CLUSTERHEADACHE AND MIGRAIN)

AND TRIGEMINALNEURALGIAdr.Made Oka Adnyana, SpS(K)

Aims :Diagnosis work up, management of primary headaches.(tension type headache, cluster headache, migraine) and trigeminal neuralgia.

Learning outcome;1. To describe the definitionof headache.2. To describe the pathophysiology of headache,3. To defrentiate primary and secondary of headache.4. To diagnosis primary headaches (tension type headache, migraine and cluster headache).5. How to manage primary headache ( pharmacology , non pharmacology), and trigeminal

neuralgia

Curiculum content.1. Nerve inervation of head.2. Pain sensitive structures of the head3. Physiology of trigeminal nociception.4. Clasification of primary headaches.5. Clinical sign and symptom of primary headaches.6. Treatment of primary headaches.



Abstracts of lecture.Headache is the most common complain in neurology medical practice. Headache divided

into primary and secondary. In differentiating both classes, we need to find the red flag sign. Secondary headache is assumed for their existence. Red flag sign are sign and symptoms those need further investigation because of their more dangerous underlined disease. Primary headache consist of tension type hedache, migraine, cluster headache and other primary headache.

To diagnosic primary headache we need more about of headache, because physical examination and laboratory result usually normal.

Treatment of primary headache consist of pharmacology (analgetic) and non pharmacology management. Treatment with analgetic must be carefully, because over use of analgetic could make a drug over use headache.

Trigeminal neuralgia is a group of symptoms characterized by severe pain attacks accompanied sudden spasm of the face in a short time, which is limited to the areas served by dermatomes of the trigeminal nerve. Between attacks there is usually pain free .Treatment of trigeminal neuralgia is with anticonvulsants and surgery

Trigger/scenario.1st case A 17 years old woman, came to the neurology clinic, with complain of headache, tight or pressing sensation on head, bilateral each episode lasts in 30 minutes – 7 days.

Learning task.1. 1.What symptom we should ask to the patient?2. What is diagnosis of this case?. 3. How to manage this patient.

2nd caseA 21 yers old boy complain of uinilteral headache since yesterday. He experienced severe pain around the eye ball. With red and watery eye as well. While having the attack in experienced vomitting, nausea. First attack was occurred at age of 20, happened 8 times/day. And finally the distance between eyelids got soaller when he had headache.

Learning task.1. What other symptom we should know to diagnose this case?.2. What could be the possible diagnosis.3. How is the management.

3rd. case.A 18 years old women complain unilateral headache since 2 days ago. She exprerienced moderat pain in the left side of head. She also experienced blured vision about 60 minute before headache. Blurred vision lasting about 10 minutes. First attack was occurred by age 15 years old. Her mother has the same symptom.

Learning task1. What other symptom we should know to diagnose this case?.2. What could be the possible diagnosis.3. How is the management.



Self assessment.1. Describe pain sensitive structure of the head.2. Describe phathophysiology of headache.3. How to defrenteate primary and secondary headache.4. Describe what is the red flag.

4th case.A 40 year sold man complaints severe pain on left side of the face especially when washing

the face, sensation of pain as such as burning and lasting a few minutes.

Learnig task.1. What other symptom we should know to diagnosis this case.2. What could be the possible diagnosis.3. How is the management.

Self assessment.1. Describe anatomy trigeminal nerve.2. Describe pathophysiology neuralgia trigemini.3. How to defrenteate trigeminal neuralgia and primary headache (cluster headache).

NEUROIMAGINGdr. Made Widhi Asih, Sp.Rad(K)

Aim :Describe the neuroimaging modalities for headache

Learning outcome : 1. Know the neuroimaging modalities for headache 2. Understand the basic principle of each neuroimaging modality3. Understand the advantage and disadvantage of each neuroimaging modality 4. Be able to choose the appropriate radiology examination for neuroimaging case

AbstractHeadache is a common clinical feature in patients in the emergency room and in general

neurology clinics. Physicians are regularly confronted with the question of whether or not it is necessary to perform neuroimaging in order to confirm a distinct headache diagnosis. For physicians not experienced in headache disorders it might be difficult sometimes to decide in which patients neuroimaging is necessary to diagnose an underlying brain pathology and in which patients cerebral imaging is unnecessary.

Headache may be caused by primary disorders, such as migraines, or secondary disorders, such as intracranial neoplasm or hemorrhage. Imaging plays an important role in differentiating between primary and secondary headache disorders. Neuroimaging including conventional and advanced radiology imaging. Each modality has advantages and disadvantages that should be considered in choose the appropriate examination for headache.



SCENARIO :

A young male came with chronic headache that getting worsen progressively, sometimes accompanied by projectile vomiting, no history of trauma previously.

Learning Task :1. What is the differential diagnosis of this patient?2. What kind of conventional radiology examination will you suggest ?3. What kind of advanced radiology examination you should suggest to performed, if from

conventional radiology showed abnormality?

Self Assessment :1. Describe the radiological sign of intracranial pressure increasing on X ray2. Describe how to prepare the patient before radiological examinations that require contrast

DAY 5th

June 1st 2016RADICULOPATHY

dr. Komang Arimbawa, Sp.S

Aim :Describe the structure of spine and relation to nerve roots. Describe clinical characteristic, risk factors , diagnostic work-up including history, clinical examination, imaging, and treatment of radiculopathy.

Learning outcome : 1. Know the the structure of spine and relation to nerve roots.2. Understand and explain how cervical and back problems induced radiculopathy.3. Be able to obtain a comprehensive history and physical examination in the assessment of

patients with radiculopathy.4. Understand the use of diagnostic tool for assessing radiculopathy5. Understand treatment of radiculopathy.

AbstractRadiculopathy is a peripheral neurologic syndrome resulting from mechanical injury and

chemical irritation of the spinal nerve roots. It may involve a single, or multiple nerve roots. Two most common types are lumbosacral and cervical. Obtaining a detailed history is important to establish a diagnosis of radiculopathy. The diagnosis may be suggested by symptoms of pain, numbness, and weakness in a pattern consistent with the distribution of a particular nerve root. Neck or back pain may also be present. Physical examination may reveal motor and sensory deficits in the distribution of a nerve root. In cervical radiculopathy, Spurling's test may elicit or reproduce symptoms radiating down the arm. In the case of lumbosacral radiculopathy, a Straight leg raise maneuver may exacerbate radiculopathic symptoms. Deep tendon reflexes may be diminished or absent in areas innervated by a particular nerve root.



Little is known about the natural history of radiculopathy. The pathogenesis involves an inflammatory process initiated by nerve root compression. Radiography of the spine is usually the first diagnostic test ordered in patients who present with neck and back symptoms. MRI has become the method of choice for imaging to detect significant soft-tissue pathology, such as disc herniation. There are few controlled randomized studies comparing operative with nonoperative treatment for this condition. There is no clear evidence that surgical treatment provides better long-term outcomes than nonoperative measures. Initial treatment should be directed at reducing pain and inflammation. The treatment can begin with local icing, NSAIDs, and measures that reduce the forces compressing the nerve root: relative rest; avoiding positions that increase symptoms; manual traction; and, if necessary, mechanical traction. Epidural steroids have been used in patients whose conditions have not had satisfactory responses to medications, traction, and a well-designed physical therapy program.Patients whose condition fails to improve with a comprehensive rehabilitation program and selective injections should be offered a surgical evaluation. Generally, patients should show progressive improvement over the first 6-8 weeks with conservative treatment. If there is no significant improvement in this time frame, consider a surgical evaluation.

Self assesment.1. What is the definition of radiculopathy ?2. Why it happened most often in cervical and lumbar spine ?3. Explain the mechanism of radiculopathy !4. Explain the diagnostic work-up for radiculopathy !

Scenario :A 20 years old man, bodybuilder complaint low back pain suddenly after trained in fitness centre. The pain is radiating pain accompanied by paresthesia that spreading to the right lateral side of thigh ntill toe. There were no micturition and defection disturbances.

Learning task :1. What is the differential diagnosis of this patient?2. If etiology of back pain in this patient is HNP (hernia nukleus pulposus) L4-L5, what is the

symptoms and signs ?3. What is diagnostic work-up for this patients ?4. What is the management for this patients?

Learning Resources :1. Eubanks JD.Cervical Radiculopathy: Nonoperative Management of Neck Pain and Radicular

Symptoms. Am Fam Physician. 2010;81(1):33-402. Last AR, Hulber K. Chronic Low Back Pain: Evaluation and Management. Am Fam Physician.

2009;79(12):1067-10743. Taylor LP, Lemming SE. Neck and Back Pain. American Academy of Neurology. 4. Ropper AH, Samuels MA, Klein JP. Pain in the Back, Neck, and Extremities. Principles of

Neurology 10th ed. 2014: 198-225

ACUTE AND REFERED PAINDr.dr.Pt. Pramana, Sp.AN., KMN.,M.Kes.



AimsDescribe mechanism and function of pain

Learning OutcomesApply its concepts and principles in acute pain patient setting

Curriculum ContentsDescribe basic mechanism of painDescribe neuronal circuit processing of painDescribe role of neurotransmitter in central and peripheral nervous system

Abstracts Of LecturesPain is a personal, subjective experience that involves sensory, emotional and behavioural factors associated with actual or potential tissue injury. What patients tell us about their pain can be very revealing, and an understanding of how the nervous system responds and adapts to pain in the short and long term is essential if we are to make sense of patients’ experiences. Although acute pain and associated responsescan be unpleasant and often debilitating, they serve importantadaptive purposes. They identify and localize noxious stimuli,initiate withdrawal responses that limit tissue injury, inhibitmobility thereby enhancing wound healing, and initiate motivationaland affective responses that modify future behavior. Nevertheless,intense and prolonged pain transmission, as well asanalgesic undermedication, can increase postsurgical/traumaticmorbidity, delay recovery, and lead to development of chronicpain. The wide area of discomfort surrounding a wound, or even a wound that has healed long ago, such as an amputation stump, is a natural consequence of the plasticity of the nervous system.An understanding of the physiological basis of pain is helpful to the sufferer, and the professional who have to provide appropriate treatment. Understanding the anatomical pathways and neurochemicalmediators involved in noxious transmission and pain perceptionis key to optimizing the management of acute and chronicpain.

According to the International Association for the Study of Pain (IASP), pain is defined as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in term of such damage. “(IASP 1979). With regard to a more recent classification, pain states maybe characterized as physiologic, inflammatory (nociceptive), orneuropathic. Physiologic pain defines rapidly perceived nontraumaticdiscomfort of very short duration. Physiologic pain alertsthe individual to the presence of a potentially injurious environmentalstimulus, such as a hot object, and initiates withdrawalreflexes that prevent or minimize tissue injury.Nociceptive pain is defined as noxious perception resultingfrom cellular damage following surgical, traumatic, ordisease-related injuries. Nociceptive pain has also been termedinflammatory 6 because peripheral inflammation and inflammatorymediators play major roles inits initiation and development.In general, the intensity of nociceptive pain is proportional tothe magnitude of tissue damage and release of inflammatorymediators.Neuropathic pain is defined by the International Associationfor the Study of Pain as “pain initiated or caused by apathologic lesion or dysfunction” in peripheral nerves and CNS.Some authorities have suggested that any chronic pain stateassociated with structural remodeling or “plasticity” changesshould be characterized as neuropathic.Neuropathic painis usually constant and described as burning, electrical, lancinating,and shooting.

Case



A 45 years old woman was admitted to emergency unit with broken left lower arm and bruishing in her left foot due to motorcycle accident. She was fully conscious. She was crying for those pain. It was so painful, she told the physician at the emergency unit. She brought to the OR for close reduction and wound toilette under general anesthesia. The anesthesiologist gave some opioid analgesic and non steroid anti-inflamation drug post anesthesia. She looks comfortable in post anesthesia care unit and discharge at the same day.

Learning TaskDescribe mechanism/pathophysiology of pain in this patient?How should we manage the pain in this patient?What is the risk of under-treatment in the acute pain patients?

Self AssesmentWhat is meant by analgesia?What is the difference between analgesia & anesthesia?What is hyperalgesia?What is a dysesthesia?What is neuroplasticity in pain and explain the mechanism?

DAY 6th

June 2nd 2016NEUROPATHIC PAIN AND NEUROPATHYDr.dr. Thomas Eko Purwata, Sp.S (K), FAAN

Aims :Know the current definition of neuropathic pain, the epidemiology, classification and etiological,

anatomical or mechanism based of neuropathic pain. Clinical characteristic ,diagnostic work-up including history, clinical examination and treatment of neuropathic pain.

Learning outcome1. Definition

Recognize that neuropathic pain is a consequence of injury or disease affeting the somatosensory system.

2. Epidemiology- Know that painful peripheral neuropathy is common complication in HIV/AIDS, diabetes,

alcoholism and vasculitis.- Know that 4 out of 5 patients with idiopathic polyneuropathy and 1 in 3 patients with Guillain

Barré syndrome have neuropathic pain - Know that peripheral neuropathic is common after surgical procedure, as well as during

treatment with chemotherapeutic agents.

3. Etiology.



- Know the common causes for neural damaged and subsequent pain i.e.: metabolic disease, infection, ischemia, injury, entrapment, connective tissue disease, AIDS, malignancy, drugs and toxins.

- Know that neuropathic pain may develop without any identifiable cause (e.g., intercostal neuralgia, idiopathic polyneuropathy).

- Know that painful neuropathy may be the first manifestation of a systemic disease. 4. Clinical characteristic of neuropathic pain

- Know the common symptoms associated with neuropathic pain e.g., burning pain, electric shock-like pain, pain paroxysm, dysesthesia and paresthesia.

- Know the common signs associated with neuropathic pain including positive (mechanical and thermal allodynia and hyperalgesia, temporal and spatial summation), negative ( sensory loss, weakness and muscle atrophy) and other signs ( neuroma signs, referred sensation, swelling, skin flare and discoloration, hyperhidrosis and trophic changes).

- Know that the patient with neuropathic pain may have concomitant non-neuropathic pain.- Know that questionnaires have been developed to differentiate neuropathic pain from non-

neuropathic pain, e.g., the LANSS Pain Scale and the Neuropathic Pain Questionnaire or to measure various characteristics, e.g., the Neuropathic Pain Scale and the Neuropathic Pain Inventory .

5. Pathological changes in nervous system- Know the pathological changes that occur the affected nerves e.g. Wallerian degeneration,

sprouting and neuroma formation.6. Know pathophysiological mechanisms in peripheral and central nervous system.7. Know diagnostic work-up including history, clinical examination and treatment of neuropathic pain.

Abstract .The new definition ofneuropathic painaccording International Association for Study of Pain

(IASP) is a consequence of injury or disease affeting the somatosensory system.For the vast majority of neuropathic pain diagnostic entities, there is no precise information about percentage of subjects reporting neuropathic pain. However it has been estimated that about 5% of patient with traumatic injury suffer from pain. Further about 8 % of stroke patients suffer from central neuropathic pain as do about 28% of patients with multiple sclerosis and about 75% of patients with syringomyelia.Neuropathic pains are classified according either to the etiological diagnosis of the neuropathy ( e.g., painful diabetic neuropathy, postherpetic neuralgia or post traumatic neuralgia), or to the anatomical site of the lesion (e.g., central or peripheral pain).Basic research in animal models of neuropathic pain indicates that multiple pathophysiological mechanism may be at play in neuropathic pain condition.

Clinical characteristic of neuropathic pain were varied. The common symptoms associated with neuropathic pain e.g., burning pain, electric shock-like pain, pain paroxysm, dysesthesia and paresthesia. The symptoms of neuropathic pain including positive (mechanical and thermal allodynia and hyperalgesia, temporal and spatial summation), negative (sensory loss, weakness and muscle atrophy) and other signs (neuroma signs, referred sensation, swelling, skin flare and discoloration, hyperhidrosis and trophic changes).

Diagnostic work-up including collection of medical history, focused at exploring the onset of pain and posssible association with current diseases, trauma, surgery etc.Therapeutic intervention applied in neuropathic pain consist of pharmacological and non pharmacological approach.



Common pharmacological approaches used for neuropathic pain including : sodium and calcium channel blocker, NMDA receptor blocker, anti depressant, anti convulsant and opioid. NSAID is not responsive for treatment neuropathic pain.

ScenarioA 55 years old man complaint parasthesia in both his legs accompanied by electric shock like pain especially in bed time. Patient refused use blanked when he sleeps although the weather is very cool , the reasons were he felt pain on his legs when contact with contact with blanked. Past history he has been suffering diabetes since 6 years ago, with un controlled blood glucose.

Learning task :1. What is the type of the pain in this patient ?2. Describe the pathophysiology of the pain in this patient.3. What is the management of this patient ?

Self assesment.1. What is the classification of neuropathic pain ?2. Explain the mechanism of neuropathic pain !3. Explain the clinical manifestation of neuropathic pain !4. Explain the management of neuropathic pain !

Learning Resource :1. Justins DM. Pain an Update Review. IASP Press, Seattle, 20052. Bonica Management of Pain, 20013. Loeser JD. The Kyoto protocol of IASP Basic Pain Terminology Pain 137 (2008), 473-74. Mogil J. Pain 2010 an Updated Review. IASP Press, seattle, 2010.

NEUROPATHYDr.dr. Thomas Eko Purwata, Sp.S(K), FAAN

Aims :Know the current definition of neuropathy, the epidemiology, classification and etiological,

anatomical or mechanism based of neuropathy. Clinical characteristic ,diagnostic work-up including history, clinical examination and treatment of neuropathy.

Learning outcome:1. To Describe the definition of neuropathy2. To describe patophysiology of neuropathy3. To describe diagnosis and differential diagnosis of neuropathy4. To describe how to manage neuropathy

Curiculum contens:1. Epidemiology of neuropathy2. Clinical presentation of neuropathy3. Risk factor of neuropathy4. Pathophysiology of neuropathy5. Diagnosis and Differential diagnosis of neuropathy



6. Treatment of neuropathy

AbstractNeuropathy is a general term that refers to diseases or malfunctions of the nerves. Any nerves

at any location in the body can be damaged from injury or disease. Neuropathy is often classified according to the types or location of nerves that are affected. Neuropathy can also be classified according to the disease causing it. (For example, neuropathy from the effects of diabetes is called diabetic neuropathy.)Types of Neuropathy arePeripheral neuropathy: Peripheral neuropathy is when the nerve problem affects the nerves outside of the brain and spinal cord. These nerves are part of the peripheral nervous system. Accordingly, peripheral neuropathy is neuropathy that affects the nerves of the extremities- the toes, feet, legs, fingers, hands, and arms. The term proximal neuropathy has been used to refer to nerve damage that specifically causes pain in the thighs, hips, or buttocks.Cranial neuropathy: Cranial neuropathy occurs when any of the twelve cranial nerves (nerves that exit from the brain directly) are damaged. Two specific types of cranial neuropathy are optic neuropathy and auditory neuropathy. Optic neuropathy refers to damage or disease of the optic nerve that transmits visual signals from the retina of the eye to the brain. Auditory neuropathy involves the nerve that carries signals from the inner ear to the brain and is responsible for hearing.Autonomic neuropathy: Autonomic neuropathy is damage to the nerves of the involuntary nervous system, the nerves that control the heart and circulation (including blood pressure), digestion, bowel and bladder function, the sexual response, and perspiration. Nerves in other organs may also be affected.Focal neuropathy: Focal neuropathy is neuropathy that is restricted to one nerve or group of nerves, or one area of the body. Symptoms of focal neuropathy usually appear suddenly

CARPAL TUNNEL SYNDROME (CTS), TARSAL TUNNEL SYNDROMEAND PERONEAL PALSY

dr. I.A. Sri Wijayanti, M.Biomed, Sp.S

Aims:Describe pathophysiology, diagnosis, early management and referral patient with CTS

Learning outcome:1. To Describe the definition of CTS2. To describe patophysiology of CTS3. To describe diagnosis and differential diagnosis of CTS4. To describe how to manage CTS

Curiculum contens:1. Epidemiology of CTS2. Clinical presentation of CTS3. Risk factor of CTS4. Pathophysiology of CTS5. Diagnosis and Differential diagnosis of CTS6. Treatment of CTS

Abstract of lectureCarpal Tunnel Syndrome (CTS) remains a puzzling and disabling condition present in 3.8% of

the general population. CTS is the most well-known and frequent form of median nerve entrapment,



and accounts for 90% of all entrapment neuropathies. The pathophysiology of CTS involves a combination of mechanical trauma, increased pressure and ischemic injury to the median nerve within the carpal tunnelThe various methods of diagnosis are explored; including nerve conduction studies, ultrasound, and magnetic resonance imaging. The treatment of CTS falls under two categories: conservative and surgical. The treatment of CTS falls under two categories: conservative and surgical

Trigger/scenarioA woman25years old present withparasthesiain the fingers ofthe right handaccompanied bypain.Complaintsbecome worsenedat night.

Learning Task.1. What other symptom we should know to diagnose this case?2. What could be the possible diagnosis?3. What is the management of this patient?

Self assesment.1. What is the definition of CTS2. Explain patophysiology of CTS3. Explain the diagnosis and differential diagnosis of CTS4. Explain the management of CTS

Learning Resource :1. Ibrahim., Khan W.S., Goddard N.,and P. Smitham, 2012. Carpal Tunnel Syndrome: A Review

of the Recent Literature. The Open Orthopaedics Journal, 2012, 6, (Suppl 1: M8) 69-76.

TARSAL TUNNEL SYNDROMEdr. IA Sri WIjayanti, M. Biomed, Sp.S

AIM: Describe the anatomy of tarsal tunnel, tibial and sural nerve, know the current definition of TTS, etiology, mechanism based of TTS, clinical characteristic, diagnostic work-up including history, clinical examination and early management of TTS.

LEARNING OUTCOMES:

1. Know the anatomy of tarsal tunnel, tibial and sural nerve2. Understand and be able explain etiology and mechanism based of TTS3. Be able to explain a comprehensive history , clinical examination and assessment of patients

with TTS. 2. Understand early management of TTS

ABSTRACTThe tarsal tunnel is a fibro-osseus space located posterior to the medial malleolus. Tarsal

Tunnel Syndrome (TTS) is an entrapment neuropathy of the posterior tibial nerve under the flexor retinaculum of the medial ankle. It is probably uncommon, but is both misdiagnosed and unrecognized because of the vagaries of the symptoms and signs and the difficulties in electrodiagnostic



confirmation. It can be confused with many sources of neuropathic and non-neuropathic foot pain or paresthesia. A Variety of test performed on physical exam as well as imaging studies improve the detection and diagnosis of TTS. Conservative therapy is initially employed in most cases without space occupying lesion. Good clinical outcomes are often reported with surgical release of the flexor retinaculum. SCENARIOA 39 years old female came to clinic with pain and burning of 5 months duration in her right ankle and sole. More recently, pain has occurred at rest waking her at night. She expressed losing ability to walk, if the pain continued to progress.

LEARNING TASK1. What other history taking, other symptoms that we should explore to diagnosis this case?2. What other examination that we should do to diagnosis this case?3. What could be the possible diagnosis?4. What is management of this patient?

SELF ASSESSMENT1. What is the definition of TTS2. Explain etiology and mechanism based of TTS3. Explain the diagnostic work- up and differential diagnosis of TTS4. Explain the treatment of TTS

Learning resourcesHerskovitz S, Scelsa NS, Schaumburg HH. Focal Neuropathies: Nerve Injuries, Entrapments, and Other Mononeuropathies. In Peripheral Neuropathies in Clinical Practice. 2nd ed. Oxford University Press; 2010:chap 18.

PERONEAL PALSYdr. IA Sri WIjayanti, M. Biomed, Sp.S

AIMDescribe the anatomy of peroneal nerve, know the current definition of peroneal nerve palsy, etiology, mechanism based of peroneal nerve palsy, clinical characteristic, diagnostic work-up including history, clinical examination and early management ofperoneal nerve palsy.LEARNING OUTCOMES:1. Know the anatomy of peroneal nerve2. Understand and be able explain etiology and mechanism based of peroneal nerve palsy3. Be able to explain a comprehensive history , clinical examination and assessment of patients with peroneal nerve palsy. 4. Understand early management of peroneal nerve palsy

ABSTRACTPeroneal nerve palsy is the most common entrapment neuropathy in the lower extremity. Most often, peroneal nerve palsy occurs at fibular neck, where the nerve is superficial and vulnerable to injury.



Patients usually present with a foot drop and sensory disturbance over the lateral calf and the dorsum of foot. The most common site of injury is the fibular head, but focal neuropathies have also been reported at the level calf, ankle and foot. Electrophysiology can localize the level of the nerve palsy, reveal the underlying pathology, and establish the prognosis.

SCENARIOA 45 years old male came to clinic with chief complaint of left leg pain. His symptoms began after she fell of on her left hip 3 months ago. He had some weakness when walking and his symptoms had progressed. The patient also complained of left-sided lower back and buttock pain with movement and intermittent “lightning bolt’ sensation to thighs.

LEARNING TASK1. What other history taking, other symptoms that we should explore to diagnosis this case?2. What other examination that we should do to diagnosis this case?3. What could be the possible diagnosis?4. What is management of this patient?

SELF ASSESSMENT1. What is the definition of peroneal nerve palsy5. Explain etiology and mechanism based of peroneal nerve palsy6. Explain the diagnostic work- up and differential diagnosis of peroneal nerve palsy7. Explain the treatment of peroneal nerve palsy

Learning Resources1. Herskovitz S, Scelsa NS, Schaumburg HH. Focal Neuropathies: Nerve Injuries, Entrapments, and Other Mononeuropathies. In Peripheral Neuropathies in Clinical Practice. 2nd ed. Oxford University Press; 2010:chap 18.2. Masakado Y, Kawakami M, Suzuki K, Abe L, Ota T, Kimura A. Clinical Neurophysiology in The Diagnosis of Peroneal Nerve Palsy. 2008. Available at www.kjm.keio.ac.jp/past/57/2/84 accessed 13 Mei 2016

DAY 7th

June 3rd 2016DEMENTIA / ALZHEIMER

Dr.dr. AA Putri Laksmidewi, Sp.S (K)

Aims : Provide initial assessment and management, established tentative diagnosis and refer patient with Alzheimer Dementia (AD) and vascular dementia (VaD)

Learning outcome : 1. Describe different types of dementia2. Describe signs and symptoms of dementia3. Explain risk factors and prevention of dementia4. Identify some tools available to assess the presence of dementia



Abstracts Dementia is defined as an acquired syndrome of decline in memory and at least one other

cognitive domain such as language, visuo-spatial, or executive function sufficient to interfere with social or occupational functioning in an alert person.Dementia involve a mental decline that affects more than one of the four core mental functions :

recent memory (the ability to learn and recall new information) language (the ability to write and speak or to understand written or spoken words) visuspatial function (the ability to see and understand spatial relationships among objects, ex :

skill needed to use a map) executive function (the ability to plan, reason, solve problems and focus on a task)

As people age there are normal changes on memory. There are changes in the way our brains store information and it is often harder to recall information. However, normal memory changes do not interfere with your ability to function on daily living. When this occurs it is not normal aging.

Mild cognitive impairment (MCI) is a transition phase between normal aging and dementia. People with MCI present with subjective memory loss and have evidence of memory impairment on cognitive testing. However, general intelligence is preserved and there are no changes in the ability to carry out activities of daily living (ADL).

Alzheimer’s disease and cerebrovascular ischemia(vascular dementia) are the two most common causes of dementia. Between 60% and 70% of individuals with dementia have Alzheimer’s disease; about 20% to 30% have either vascular dementia or a combination of vascular dementia and Alzheimer’s disease.

A definitive diagnosis of dementia alzheimer is possible only through brain autopsy, so completing a thorough assessement encompassing many components lends to the best probable diagnosis. Assessment for dementia includes history from patients, history from a reliable family member (caregiver), physical examination, cognitive assessment and functional assessment. Laboratory and imaging test are used to rule out reversible causes of dementia.

Scenario 1 :A 60-years-old man, came to the hospital with difficulty in memory. This patient had a 6-months history of memory impairment. He has been a cerebrovascular diseases (stroke) since a year ago. He has been a high blood pressure and diabetes mellitus.

Learning Task :1. How to diagnose this patients?2. How to differentiate this patients?3. Please explain the etio-pathogenesis and pathophysiology4. What test should be used ?

Self Assessment :3. Describe taking a good history on the memory impairment4. Describe the neurologic and neurobehaviour examination 5. Describe the causes of dementia 6. Describe how to manage this dementia7. Describe the prognosis for this patient

Scenario 2 :



A 60 years old woman came with complaint of slowly progressed memory and cognitive impairment approximately since 5 years ago.He has not been a high blood pressure or head injury.

Learning Task :1. How to diagnose this patients?2. How to differentiate this patients?3. Please explain the etio-pathogenesis and pathophysiology4. What test should be used ?

Self Assessment :1. Describe taking a good history on the memory impairment2. Describe the neurologic and neurobehaviour examination 3. Describe the causes of dementia 4. Describe how to manage this dementia5. Describe the prognosis for this patient

MOVEMENT DISORDERS/NEUROGERIATRICDr dr DPG Purwa Samatra Sp S(K)

Movement disorders are commom in clinical practice. Movement. Movement disorders divided, based on movement type. Based on these movement disorders divided : hyperkinetic movement disorders and hypokinetic movement disorders.

Hypokinetic : Akinesi/bradykinesis Rigidity Postural Instability Stiff-man syndrome/freezingHyperkinetic : Chorea Myoclonus Dystoniia Tics Tremor

PARKINSONISMParkinsonism is a syndrome manifested by a comination following six cardinal features. A combination of these signs is used to clinically define : definitte, probable and possible.

Parkinson disease (PD) , first rcognized as a unique clinical entity by James Parkinson in 1817, who in his An Essay on the Shaking Palsy.

Diagnostic criteria of Parkinsonism1. Tremor at arest2. Bradykinesia3. Rigidity4. Postural instability



4. Flexor position5. Freezing ( motor blocks)

Definite : At least two of these features must be present, one of them being 1 or 2Possible : At least two of feture 3 to 6 must be presentProbable: Feature 1 or 2 alone is present

Etiologi : Common causes of Parkinsonism :

1. Idiopathic Parkinson Disease ( primary )2. Drug-induced Parkinsonism ( secondary Parkinsonism)3. Multiple system atrophy4. Progressive supranuclear palsy

PathogenesisParkinson desease and Parkinsonism doe to degeneration of substansia nigra ( part of basal ganglia), with a resulting deficiency of striatal dopamine. Clinical features begin to emerge when approximately 60% loss dopamine.Another sgn of Parkinsonism are non motor symptom : autonomic dysfunction, cognitive abnormalitas, sleep disorders, depressive disorders, gastrointestinal abnormalit Pathophysiology of Parkinonism : decrease of dopaminergyc neurons at substantia nigra, as a part of basal ganglia. The basal ganglia comprice four structures: The striatum( putamen,nucleus caudatus), the pallidum, the subthalamic nucleus and nigral subtstance.

The Hoehn & Yahr Scale: the common way to rate progression of symptoms in PD (17)

1. Stage one1. Sign and symptoms on one side only2. Symptoms mild3. Symptoms inconvenient but not disabling4. Usually presents with tremor of one limb5. Friends have noticed changes in posture,

locomotion and facial expression.2. Stage two

1. Symptoms are bilateral2. Minimal disability3. Posture and gait affected

3. Stage three1. Significant slowing of body movements2. Early impairment of equilibrium on walking or

standing3. Generalized dysfunction that is moderately severe

4. Stage four1. Severe symptoms2. Can still walk to a limited extent3. Rigidity and bradykinesia



4. No longer able to live alone5. Tremor may be less than earlier stages

5. Stage five1. Cachetic stage2. Invalidism complete3. Cannot stand or walk4. Requires constant nursing care

TreatmentTreatment of Parkinsonism :

1. Medical treatment2. Surgical treatment/ invasive treatment

Medical treatment : 1. Increase dopamine level : l-dopa ( levodopa), carbidopa, benzerazide, ,COMT

inhibitor( catechol-O methyltransferase inhibitor : entacapone), type B MAO inhibitor (selegiline).

2. Dopamine agonist : pramifeksole3. Anti cholenergic : trihexyphenidyl

Surgical treatment :1. DBS : deep brain stimulation2. Pallidotomy

Rehabilitation: Physical, accupational.

References : 1. Parkinson Disease and Movement Disorders by : T.N Mehrotra, Kalyan B.Bhattachharyya.2. Principles and Practice of Moveement Disorders by : Stanley Fahn, Joseph Jankovic, Mark

Hallet

Trigger / scenarioA 62 year old man, Balinese, Hinduism came to hospital with main complaint tremble of both hand since six month ago. On examination we found resting tremor on the right hand more severe then left hand.

1. What are other things that have to be asked in this patient?2. What are the physical examination that you should look in this patient ?3. How to make proper diagnosis in this patient ?4. What is your diagnostic procedures suggestion ?5. What is diffrential diagnosis of this patient ?6. What is the management of this patient ?7. What other education should be given to this patient ?8. When this patient should be referred to neurologic expertise?

Learning task.



1. Please describe what is Parkinsonism and what is Parkinson “s disease (PD ) ?2. What are the pathology and pathogenesis of PD ? 3. Please describe pathophysiology of PD.4. What are diagnostic criteria in PD?5. Please describe management of PD.6. Please describe differential diagnosis of PD.7. Please describe how you can differentiate PD with symtomatic Parkinsonism ?8. Please describe how you can differentiate PD with Paekinsonism Plus ?

Self assesment1. Please describe basal ganglia component.2. Please describe circuit of basal ganglia.3. Please describe role of neurotransmitter in basal ganglia.

Abstract of lecturesInvoluntary movementInvoluntary movement have certain common properties ;

- In most case the type of movement is recognized by observation.- Involuntary movement are often accentuated by stress.- Involuntary movement disappear during sleep.Classification of involuntary movement including

chorea, athetosis, ballismus, dystonia, tremor, mioclonus and tics.The most pathologic sites responsible for the involuntary movement reside in basal ganglia like chorea, athetosis, ballismus. Each movement disorder has multiple etiologies but shared pathophysiologies and phenotype.Management of involuntary movement is symptomatic and causal therapy.

Trigger/ scenarioA 14 years old Balinese female, Hinduism, came to hospital with main complaint her right hand and fingers was moving since yesterday and cannot stopped , followed by geadual involvementof the upper limb and spread to her face and her tongue. She had history of pain in her knee 3 month ago.

1. What shoul tou ask to the patient or her family if chief complaint ts involuntaey movement?2. What physical examination should be to do to this patient ?3. What do you think about the diagnosis of the patient ?4. What are the diagnosis criteria in this patient ?5. What are diagnostic procedure you will suggest for this patient ?6. What are the differential diagnosis of this patient ?7. What medication should be given to this patient ?8. How is the prognosis of this patient ?

Learning task1. Please describe pathogenesis of chorea athetosis.2. Please describe pathogenesis dystonia3. Please describe pathogenesis of Ballismus

Self assesment1. Plase describe circuit three of basal ganglia2. Please describe definition of chorea, athetosis, ballismus, dystonia, tremor and tics. 3. Please describe how to manage each involuntary movement.



4. Please describe the kind of tremor.

DAY 8th

June 6th 2016CENTRAL NERVOUS SYSTEM TUMOR

dr. Made Susilawathi, Sp.S

AbstractTumor of the nervous system comprise a diverse, heterogeneous group of neoplastic lesions

that affect every age group and every element of the central nervous and peripheral nervous system. Most CNS tumors are thought to be sporadic in origin, tumors arise as a result of combined somatic mutation that active oncogenes such as platelet-derived growth factor and inactivate tumor suppressor genes as p53. The role of environmental factors –physical,chemical, or infectious- in causing such mutations or otherwise acting as risk factor is as yet unclear. There are two types of tumor, 80 % of all tumors are primary tumors and 20 % are metastatic . Typical presenting signs are headache, seizure, focal neurologic deficit and non specific cognitive and personality changes that follow a subacute course. Detailed neurologic examination can localize lesions within the CNS. Imaging tests are essential to direct further diagnostic and management strategies. Surgical biopsy is almost always required for conclusive diagnosis. A female, 30 years old, government employee, came to the neurologic ward who has been suffering from blur and double vision for about two weeks and getting worst. She has also severe headache, nausea and vomiting since eight months ago.

Learning task1. What is the differential diagnose of this case ?2. What is the most signs and symptoms appearance in the brain’s tumour ?3. Mention of signs and symptoms the brain tumour depend on the location such as:

a. Lobus frontalesb. Lobus temporalesc. Lobus parietalesd. Lobus occipitalse. Suprasellar

4. Explain the classification of the brain tumour according to original cell of the tumour !5. If the patient suffering from metastase tumour where is the primary source ?6. If the patient is man,where is the primary source ?7. What kind the diagnostic tool to examine the process of space occupying lesion ?8. How to manage of the brain tumour ?9. How is the prognose of the brain tumour ?

Self assessment1. Student be able to explain the classification brain and spine tumour2. Student be able to explain the insidence of brain tumour in adult and children3. Student be able to explain sign and symptom of brain tumour according to part of the brain

involved4. Student be able to explain diagnostic tool to assess brain and spine tumour5. Student be able to explain how to manage the basic treatment of brain and spine tumour



6. Student be able to explain when to refer patient with headache which is suspected brain tumour

TRAUMATIC BRAIN INJURY, EDH, SAHProf. Dr. dr. Sri Maliawan, SpBS(K)

Aims:To understand traumatic brain injuryLearning Outcome

1. Comprehend the specific principles of anatomy and physiology related to brain injury.2. Identify and discuss the principles of general management of unconscious patient.3. Outline the method of evaluating head injury using a minineurologic examination 4. Identify and discuss the management techniques of head injury.

Curriculum contents:1. Scalp hematoma2. Skull fracture3. Monroe kelli doctrine.4. Glasgow coma scale5. Intracranial hematoma6. Cushing response7. Minineurologc examination8. Brain death9. Ct scan10. External and internal decompression . Abtract of lectures

IncidenceNeurotrauma is responsible for 70% of all road fatalities and 50% of trauma deaths. Road crashes cause 50- 60% of all head injuries. Accidental injury is the third highest cause of death in motorised countries. The highest incidence for hospital admission in persons under 45 years of age is form trauma.

Factor in the Rural EnvironmentThe following factors are significant in rural trauma : asolation and distance, medical facilities, level of neurosurgical competence, delay in definitive care, administrative organisation, rural crash profiles, e.g., incidence of 40% fatality on admission, more severe injuries, multiple injuries, higher incidence of single vehicle crashes, road and environmental conditions, driver competence and fatigue and compliance with preventive measures such as alcohol, seatbelts, helmets and speed.

NEUROTRAUMAClinical factors adversely influencing outcome [death and disability]

- Severity of Primary Injury- Intracranial Complications- Hypoxaemia- Hypercarbia- Hypotension- Anaemia- Multiple Injuries



- Age- Prolonged Prehospital Time- Admission To Inappropriate Hospital- Delayed Or Inappropriate Interhospital Transfer/ Retrieval- Delay In Definitive Surgical Treatment

Learning Task

Head InjuryFemale 40 years old a pedestrian was hit by motor bike , upon arrival to emergency department, she able to open her eye and say painfull while she withdrawn her hand , there are brill hematoma, rinorhea, and bloody discharge from her nose and mouth, respiratory rate 26x/mnt gurgling, Blood pressure 80/60 mmHG, and Heart rate 120x/mnt.1. What is the clinical diagnosis base on GCS.2. Initial management3. Sign of skull base fracture4. Sign and symptom of intracranial hematoma5. Mention and explain about EDH,SDH,ICH,SAH, IVH.

Self assessment1. What is cushing respons2. Craniotomy, craniectomy3. Lucid interval4. Lateralization or hemisyndrome5. Brain death

Learning resourse1. Sri maliawan cedera kepala2. American college of surgeon ; ATLS3. The neurosurgical society of Australia; head injury an remote area

Functional NeurosurgeryProf.Dr. dr. Sri Maliawan SpBS(K)

Aims:To understand traumatic functional neurosurgeryLearning Outcome

1. Comprehend the specific principles of anatomy and physiology related lesion, irritation and dysfunction

2. Identify and discuss the principles of general management ablative and non ablative procedure.3. Outline the basic principal of stereotatic, Deep brain stimulation, surgery for epilepsy and Pulse

radio frequency (PRF).

Curriculum contents:1. Surgery for Pain ( ablative and non ablative)2. Surgery for epilepsi



3. PRF4. Ab5. Micro vascular decompression (MVD) for Trigeminal neuralgia6. MVD glossopharyngeal neuralgia7. Carpal tunnel syndrome ( CTS)8. DBS9. Cervical Neuropathy and Myelopathy.10. Lumbal disc herniation

Learning TaskTrigeminal neuralgia (TN)

Female 50 years, suffering from terrible lancinating pain on and off , at the right side of his face, pain getting worst when he smile or drink water and he almost canot be able to eat. What is the clinical diagnosis 1. Initial management2. Deffrential dx3. Mention the sign and symptom of TN4. Mention and explain modality of treatment

Self assessment1. What is DBS2. Glosopharyngeal neuralgia3. Entraphment syndrome4. Example of ablative procedure for pain5. Treatment of lumbal disc herniationLearning resourse

1. Headache Classification Committee of the International Headache Society. Cephalgia. 2013. Jul; 33 (9): 629-808

2. Gronseth G, Cruccu G, Alksne J, Argoff C, Brainin M, Burchel K, Nurmikko T, Zakrzewska JM. The Diagnostic evaluation and treatment of trigeminal neuralgia (an evidence based review): report of quality stabdards subcommittee of the AAN and EFNS. Neurology. 2008; 71(15):1183.

3. Wiffen PJ, Derry S, Moore RA, Kalso EA. Carbamazepine for chronis neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev. 2014;4: CD005451

4. Jannetta PJ, Microsurgical management of trigeminal neuralgia. Arch Neurol. 1985;42(8):8005. Barker FG, Jannetta PJ, Bissomette DJ, Larkins MV, Jho HD. the long-term outcome of

microvascular decompression for trigeminal neuralgia. N Engl J Med.1996;334(17):1077

DAY 9th

June 7th 2016STROKE

dr. AABN. Nuartha, Sp.S(K):

Aims:Describe diagnosis, management and referral patients with stroke.

Learning outcome:



Describe pathogenesis, clinical aspect, examination, and management patient with stroke.

Curriculum contents:1. Ischemic stroke.2. Haemorrhagic stroke.

Abstract of lectures:Stroke is a clinical diagnosis made on the characteristic temporal profile of neurological symptoms and signs, as examplified by the WHO definition : Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer, or leading to death, with no apparent cause other than of vascular origin.Stroke is the third most common cause of death worldwide (after coronary heart disease and all cancers combined) and the major cause of disability.The most frequent cause of stroke is a localized disturbance of cerebral circulation, i.e., cerebral ischemia/infarction (ischemic/non haemorrhagic stroke). Ischemic stroke classification is base on five subtype: large artery atherothrombosis-thromboembolism, embolism from the heart, small vessel disease, uncertain cause, and rare causes. Less common are haemorrhagic stroke (spontaneous intra cerebral haemorrhage and subarachnoid haemorrhage). Subarachnoid hemorrhage is the exception to this definition and usually presents without focal neurological deficits.Stroke typically manifect abruptly, resulting in a maximum deficit usually within hours and lasting longer than 24 hours. If a patient’s focal neurological deficit lasts less than 24 hours, it is arbitrarily defined as a TIA (transient ischemic attack). Clinical history, examination and investigation will separate infarction and haemorrhage.When a clear account of symptoms is available, the clinical diagnosis of stroke works well and the risk of mistaking a nonvascular lesion for stroke is very small. When the history is not so clear, however, because the patient is unconscious, confused, or aphasic and the event has no reliable withness, the diagnosis is more difficult and the chance of misdiagnosis is high. In these situations, CT (computed tomography) or MRI (magnetic resonance imaging) is important to exclude non-stroke diagnoses such as traumatic subdural haematomas or malignancy.Treatment aims, prevent progression of present event, prevent immediate complication, prevent the development of subsequent event, rehabilitation and stroke prevention.

Trigger/scenario:A 53 years old women with a history of type 2 diabetes mellitus and atrial fibrillation pressents to the emergency room with slurred speech and right body weakness. The onset was sudden while she was swimming 1 hour ago, and she was brought immediately to the emergency room. Physical exam findings include blood pressure of 95/70 and irregularly irregular heartbeat. GCS 15. Paralysed from the right side of the body, with the face and upper extremity being worse than the lower extremity. Routine chemistries and cell counts are normalSelf assessment:

1. What is the possibility diagnosis of this patient ?2. What is the diagnosis tools you made to make definited diagnosis ?

Learning Task1. Pathogenesis of stroke.2. Clinical aspect and diagnostic tool of stroke



3. Management and prevention of stroke.

STROKE (SURGICAL MANAGEMENT)dr. I Wayan Niryana, M.Kes, SpBS(K)

AIMS:Provide initial assessment and management, established tentative diagnosis, proposed definitive management, and prognosis patient with CVA.

LEARNING OUTCOME:The student know what is the surgical indication of CVA

CURRICULUM CONTENTS:Cerebrovascular Accidents (CVA)

1. Etiology and Pathophysiology of Cerebrovascular disease2. Clinical Features and Investigations of Cerebrovascular disease3. Management and Surgical Indication for Cerebrovascular disease

ABSTRACTS OF LECTURESDue to the improvement of the treatment of ischemic heart disease over ischemic or

hemorrhagic brain disease over the last 10 years, more and more patients can benefit from non surgical and surgical intervention. The nineties have been called the decade of the brain in developed countries where brain attack has been treated as aggressively as heart attacks. Thus it is now the time for all developing countries to follow the same pathway.

Next to heart disease and cancer, cerebrovascular disease is the most frequent cause of death in the western world. And at least one-half of all neurological patients in general have some type of cerebrovascular disease. The term cerebrocvascular disease denotes any abnormality of the brain resulting from a pathologic process of blood vessels, be they arteries, arterioles, capillaries, veins, or sinuses. The pathologic change in the vessels takes the form of occlusion by thrombus or embolus, or of rupture, and the resulting abnormalities in the brain are of two types: ischemia, with and without infarction, and hemorrhage. Rarer forms of cerebrovascular disease are those due to altered permeability of the vascular wall and increased viscosity or other changes in the quality of blood. The latter changes underlie the strokes that complicate diseases such as sickle-cell anemia and polycythemia and account for the headache, brain edema, and convulsions of hypertensive encephalopathy.

From all of Cerebrovascular accidents 25% present with intracerebral haematoma (ICH) and account for 2-4% of all deaths. They are twice as common as SAH. Over two thirds are known to be fatal. The patients are usually middle aged or over, with a male preponderance. The incidence is about 1 per 10,000 with a 30day mortality of 44%. Etiology: There are two categories, primary and secondary.

Primary ICH:It is associated with hypertension and distinct from hemorrhagic infarcts. It has been suggested that hypertensive changes in the arterial wall, such as, hyaline degeneration, and micro aneurysms are at fault. Another suggestion is the thin walled vessels (such as lenticulostriates), originating directly from



the main vessel are subjected to higher intravascular pressure than the cortical vessels and tend to rupture. Eighty percent of them are supratentorial. Mostly, the location is central and deep. Secondary ICH:It is associated with a medical condition other than hypertension, representing about 20% of all ICHs. They may be due to:Coagulopathies (10-15%)-Among these, platelet disorders are important. About 5% of those receiving heparin, irrespective of the dosage, develop thrombocytopenia. The platelet defects may be hereditary (Von Willebrand’s disease) or acquired through drugs (Aspirin, penicillin, or new cephalosporin’s) or through disease (myeloproliferative and dysplastic disorders, uremia, cirrhosis, SLE, multiple myeloma).Arterio Venous Malformations (AVMs (7%) represent a heterogeneous group with different histological types (cavernoma, AVMs, venous angioma and capillary telangiectosis).Vasculopathies (5%), such as cerebral amyloid angiopathy, polyarterites nodosa and necrotizing vasculopathy in drug abusers, tend to produce multiple subcortical haematomas.Tumors (2%) such as glioblastoma and metastasis tumors such as, melanoma, choriocarcinoma, renal cell carcinoma and bronchogenic carcinoma, are the most frequent tumors in producing ICH. Pathophysiology: The haematomas may be massive (>5cm) with extension into the ventricles or may be small (<1.5 cm). The extravagated blood forms a roughly circular or oval mass which grows in volume for a brief period. Adjacent brain tissue is displaced and compressed resulting in extensive edema and ischemia. Ischemic area may be much larger than the area of clot.Cerebellar and brainstem ICH may produce obstructive hydrocephalus which may add to the problems. In large hemorrhage, there is midline shift and the vital centers are compromised. Rebleeding is rare. Resolving haematomas may develop into a cyst over a period of months, with a gliotic wall which may be orange colored due to haemosiderin laden macrophages. Clinical features: It depends on the site and size of the hematoma. Sudden headache, vomiting with depressed level of consciousness and focal signs is the usual mode of presentation. Absence of neck stiffness may help to exclude SAH. The large ones are usually associated with LOC.In putaminal ICH, the patient develops sudden hemiplegia with conjugate horizontal gaze deviation towards the clot. Speech may be involved if the dominant hemisphere is involved.In thalamic ICH, the findings are as in putaminal ICH; in addition, there may be neck retraction, paralysis of vertical gaze with upward gaze palsy, inequality of pupils, and skew deviation with the contra lateral eye being displaced downward and medially.Cerebellar ICH presents with severe headache, nausea and vomiting and imbalance and depressed level of consciousness.Pontine ICH present with coma, pin point pupils and decerebrate rigidity.Cortical ICH may present with headache and seizures. Investigations: CT Scan will reveal the clot and other associated features such as midline shift and hydrocephalus. A contrast CT may suggest a vascular problem, which may necessitate an angiography.MRI gives a better delineation of the above; in addition the age of the haematoma can be guessed. MRI may suggest an associated AVM. Angiography should be carried out whenever there is a suggestion of vascular malformation, in the absence of previous hypertension or coagulopathies before a life saving clot evacuation. When surgery is not planned, the angiography can wait for few weeks to avoid a false negative angiography.



Coagulation studies must be done as a routine in addition to ECG, chest X-ray and other general investigations.Management: Supportive care control of hypertension, reduction of ICP without compromising the CPP and prevention of complications are the mainstay. Fluid and electrolytes and tissue oxygenation must be closely monitored. The aim is to avoid secondary events.An aggressive decrease of high BP may lead to cerebral ischemia. Ideally, it should not be lowered below 150mm Hg systolic and 100 mm of Hg diastolic. Should general measures to control the raising ICP fail, hyperventilation may help; but must be employed with careful watch on pCo2, arterial blood pressure and preferably with ICP monitoring as well. The CPP should not be compromised. Osmotherapy with mannitol may help only when the serum osmolality is lower than 300 mosm/kg.Prophylactic anti convulsant therapy is advised by most physicians with no supporting evidence. The role of surgical intervention is controversial. Neurosurgeons and neurologists advocate that large cerebellar hemorrhages with compression of the brain stem or obstruction of the fourth ventricle should be surgically removed as soon as possible. Surgical removal of large lobar hemorrhages in young patients who are clinically deteriorating has also been recommended based on anecdotal experience. On the other hand, the results of such surgery in hematomas within the basal ganglia and other deep structures are unacceptable. Standard craniotomy for surgical removal of primary brain stem or thalamic hemorrhages has been all but abandoned because of the extremely poor outcomes in almost all patients.Craniotomy: Craniotomy and evacuation of the clot has been the standard approach for removal of intraparenchymal hemorrhage. In addition a decompressive craniectomy with a duraplasty is preferred by some. Its major advantage is adequate exposure to remove the clot. It is not difficult or time-consuming. The major disadvantage of a more extensive surgical approach is that it may lead to further brain damage, particularly in patients with deep-seated hemorrhages. In addition, the effectiveness of clot removal by craniotomy is far from ideal.There have been numerous nonrandomized series comparing craniotomy and best medical treatment of ICH. Recently Morgenstern and colleagues reported a single-center, randomized trial (STICH Trial) of standard craniotomy versus best medical therapy in patients with supratentorial ICH; the goal was to perform surgery 12 hours after symptom onset. Patients had to have a supratentorial ICH with a volume 10 cm3 and a GCS score of 5 to 15. Of the 34 patients in the randomized trial, 17 were randomized to removal of the ICH by standard craniotomy. The median time to surgery for the 17 patients was 8.3 hours (minimum 3.75 hours and maximum 26.1 hours). The 6-month mortality for the surgical group was 17.6% compared with 23.5% for the medical group. The median 6-month Barthel index score for survivors in the surgical group was also similar to the median Barthel index score for the medical group. However, the groups were not balanced with regard to ICH location. Only 1 of the 17 patients (6%) in the surgical group had a lobar hemorrhage compared with 7 of 17 patients (41%) of the medical group.Nonrandomized treatment series of patients with cerebellar hemorrhage report good outcomes for surgically treated patients who have large (>3 cm) cerebellar hemorrhages or cerebellar hemorrhages with brain stem compression or hydrocephalus. In these patients, medical management alone often results in bad outcomes. Smaller cerebellar hemorrhages without brain stem compression that are managed medically do reasonably well.Outcome: The natural course of spontaneous ICH leads to a 30-day mortality rate of 45% . The patient's initial level of consciousness, hemorrhage size, and intraventricular extension of blood has proven to be accurate predictors of outcome. Less commonly, age, sex, hypertension, and mass effect may indicate harmful effects on outcome in patients with ICH.



The author recommends that patients with smaller hematomas who are alert, stable, or improving should be treated medically and the patients with larger hematomas who show progressive neurological deficit, prolonged functional impairment, and intracranial hypertension should be treated surgically. Patients with a GCS score <4 should also be treated medically because they uniformly die or have extremely poor functional outcome that cannot be improved by surgery. Easily accessible supratentorial hematomas with mass effect, especially in the young and in those with a GCS score >5, must be evacuated. The aim of surgery should be the removal of as much of the clot as possible, with minimal disruption of surrounding brain tissue. If possible, surgery should also remove the underlying cause of hemorrhage, such as an arteriovenous malformation, and prevent complications of ICH such as hydrocephalus and mass effect of the blood clot. More complete clot removal may decrease elevated ICP and local pressure effects of the blood clot on the surrounding brain. Stereotactic aspiration may be associated with better outcomes than standard craniotomy; but this hypothesis has yet to be tested in a randomized study. Ultra-early removal of ICH by localized, minimally invasive surgical procedures is promising but untested. Further study of the dynamics of hemorrhage and additional results are needed prior to making a decision on how to divide patient management into the two categories of surgical and nonsurgical treatment.SCENARIO

Male patient, 50 years old was referred to the Emergency room on a face mask oxygenation, with Infusion lines at right arm with large caliber of needle, warmed crystalloids has been administered. The blood pressure is 180/100 mmHg, heart rate 60x/mnt, Respiration rate 20x/mnt. Pupil round an equal, size: right side 5mm, left side 3mm, with left hemi paresis. His eyes are open with pain stimuli and his GCS was E2V2M4. History: When he was watching TV, suddenly he got severe headache, vomiting and then seizure. After that he looks decreased of consciousness. History of hypertension (+) since 5 years ago, regularly take medication.

LEARNING TASKS1. What is the clinical diagnosis and differential diagnosis?2. What is the investigation that need for this patient?3. How is the initial management for this patient?4. When should you suggest to doing surgery for this patient?5. How should you explain the prognosis of the patient to the family?

SELF ASSESMENT1. Explain the Cerebrovascular Anatomy that supplies the brain and cerebellum.2. Learn about clinical features, investigations and differentials diagnosis of cerebrovascular

disease.3. Learn about emergency management: medical and surgical aspect of CVA.4. Learn about how to explain the prognosis of CVA.

DAY 10th

June 8th 2016TRAUMA MEDULA SPINALIS, COMPLETE SPINAL TRANSECTION,

ACUTE MEDULLA COMPRESSIONDr. dr. Tjokorda GB Mahadewa, M.Kes, Sp.BS(K)Spinal



Trauma Medula SpinalisAims:Provide initial assessment and management, established tentative diagnosis, proposed definitive management, and rehabilitation method or refer patient with Spine and Spinal Cord Injury

Learning outcome:The student can provide initial assessment and management, established tentative diagnosis, proposed definitive management, and rehabilitation method or refer patient with Spine and Spinal Cord Injury

Curriculum contents:Spine and Spinal Cord Injury:

4. Evaluate and appropriately manage for suspected Spinal Injury5. Determine appropriate patient disposition and definitive management for Spinal Injury6. Proposed rehabilitation method or refer patient with Spinal Injury

Abstracts of lecturesIt is estimated that the prevalent population of people in America with a spinal cord injury (SCI)

is approximately 200.000-400.000 people. The incidence is about 40 per million people and about 11.000 new cases per year. SCI is caused by both trauma and by disease processes (non-traumatic SCI) such as spinal cord infection and infarction. Mostly (50,7%) affected cervical level, frequently at C5 level, using American Spinal Cord Injury Association (ASIA) Impairment Scale is determined 49% in ASIA A (Complete Impaired). Typically people who acquire a traumatic SCI are young and male, whilst non-traumatic SCIs occur more often in later life and with a more even gender split. Most spinal cord injury causes permanent disability or loss of movement (paralysis) and sensation below the site of the injury. Paralysis that involves the majority of the body, including the arms and legs, is called quadriplegia or tetraplegia. When a spinal cord injury affects only the lower body, the condition is called paraplegia. Many scientists are optimistic that important advances will occur to make the repair of injured spinal cords a reachable goal. In the meantime, treatments and rehabilitation allow many people with spinal cord injury to lead productive, independent lives.

Today, there's still no way to reverse damage to the spinal cord. But modern injuries are usually less severe, partial spinal cord injuries. And advances in recent years have improved the recovery of people with a spinal cord injury and significantly reduced the amount of time survivors must spend in the hospital. Researchers are working on new treatments, including innovative treatments, prostheses and medications that may promote nerve cell regeneration or improve the function of the nerves that remain after a spinal cord injury. In the meantime, spinal cord injury treatment focuses on preventing further injury and enabling people with a spinal cord injury to return to an active and productive life within the limits of their disability. This requires urgent emergency attention and ongoing care.

Emergency actionsUrgent medical attention is critical to minimizing the long-term effects of any head or neck trauma. So treatment for a spinal cord injury often begins at the scene of the accident. If you suffer a head or neck



injury, you'll likely be treated by paramedics and emergency workers who will attend to three immediate concerns:

Maintaining your ability to breathe Keeping you from going into shock Immobilizing your neck to prevent further spinal cord damage Emergency personnel typically immobilize the spine as gently and quickly as possible using a

rigid neck collar and a rigid carrying board, which they'll use to transport you to the hospital. In the emergency room, doctors focus on maintaining your blood pressure, breathing and neck stabilization and avoiding possible complications, such as stool or urine retention, respiratory or cardiovascular difficulty, and formation of deep vein blood clots in the extremities. You may be sedated so that you don't move and sustain more damage while undergoing diagnostic tests for spinal cord injury. If you do have a spinal cord injury, you'll usually be admitted to the intensive care unit for treatment. You may even be transferred to a regional spine injury center that has a team of neurosurgeons, orthopedic surgeons, spinal cord medicine specialists, psychologists, nurses, therapists and social workers with expertise in spinal cord injury.

Early stages of treatmentIn the early stages of paraplegia or quadriplegia, your doctor will treat the injury or disease that

caused the loss of function. Immediate treatment may include: Medications. Methylprednisolone (Medrol) is a treatment option for acute spinal cord injury.

This corticosteroid seems to cause some recovery in people with a spinal cord injury if given within eight hours of injury. Methylprednisolone works by reducing damage to nerve cells and decreasing inflammation near the site of injury.

Immobilization. You may need traction to stabilize your spine and bring the spine into proper alignment during healing. Sometimes, traction is accomplished by placing metal braces, attached to weights or a body harness, into your skull to hold it in place. In some cases, a rigid neck collar also may work.

Surgery. Often, emergency surgery is necessary to remove fragments of bones, foreign objects, herniated disks or fractured vertebrae that appear to be compressing the spine. Surgery may also be needed to stabilize the spine to prevent future pain or deformity. Controversy exists regarding the best time to perform surgery. Some surgeons believe it should be performed as soon as possible in most circumstances, while others believe it's safer to wait for several days before attempting any surgery. Research has not clearly proved which approach is better.

Persisting SCI impacts on every aspect of a person's life: health status, physiological, active community participation, psychological, social, reproductive, economic, employment, educational and recreation. An SCI will affect people in variable ways, depending on the level of the spinal cord lesion and the completeness of the injury. Generally all people with SCI have some degree of motor or sensory loss and a disrupted autonomic nervous system. This has a profound effect on a person's health, function and physiology. The most important factors predicting functional outcome are the neurological level and degree of completeness of spinal cord lesion. However, a range of other medical and non-medical factors can influence outcome, including age, body shape and weight, associated injuries, pre-existing disease, spasticity and contractures, living arrangements and family support, level of education and financial resources. Functional goals are based on sequential organization of spinal segments and capacity of spared muscle groups to perform specific activities of daily living, qualified by other factors such as those listed above.

When working with patients to establish wheeled mobility goals, it is essential to understand the individual impact of a person's SCI and other health issues associated with co-morbid conditions and



with ageing. Pre-morbid lifestyle and interests, personality characteristics and coping style, degree of social support and economic circumstances will all be important factors influencing adjustment and eventual outcome. Within the learning modules is information about establishing and assessing a patient’s health status. For people who require wheeled mobility, the effective prescription and use of a wheelchair enables and empowers them to participate in life and interact in their community. Many patients with a spinal cord injury will spend most of their waking hours in their wheelchair; each patient is unique and has highly individual and, over time, changing needs. It is no longer acceptable, if it every was, to prescribe a wheelchair and seating system without careful consideration of the patient’s goals and postural, pressure, functional, safety and environmental needs. A correctly prescribed wheelchair and seating system will optimize function, address the impact of environmental factors, correct and prevent postural and pressure issues and meet a patient's community participation needs

ScenarioMale patient, 25 years old as a passenger of a public transportation, had a head on collision.

The driver was died immediately at the scene. The patient was referred to the Emergency room as being immobilized on a long spine board and semirigid cervical collar. On a face mask oxygenation, with Infusion lines at both arms with large caliber of needles, warmed crystalloids has been administered. The blood pressure is 85/40 mmHg, heart rate 130x/mnt, Respiration rate 40x/mnt, shallow respiration pattern, with an obvious injury on the chest wall. His eyes are open and well respond to verbal stimuli. He can lift up his shoulder but cannot elevate his elbows neither his legs.

1. What is the working diagnosis?2. How is the prompt management for this patient?3. How should you explain the prognosis of the patient to the family?

Learning tasks1. Learn about Initial Assessment and Management for Spinal Injury.2. Learn about Spinal Injury diagnosis and management for Spinal Injury.3. Learn about rehabilitation methods for Spinal Injury.4. Learn about how to refer patient with Spinal Injury

Self assesment1. Mention several types of Spine Fractures!2. How can we prevent Secondary Spinal Cord Injury?

MODUL: SURGICAL ASPECT OF BRAIN TUMORSDr. dr. Nyoman Golden, SpBS (K)

AimsDescribe the surgical management of brain tumors

Learning outcomesUnderstanding the surgical principles in the management of brain tumors



Curriculum 1. Preoperative management2. Perioperative management3. Operative management4. Complications

Abstract of lectureBefore embarking surgical tumor removal, evaluation of clinical history and findings, the results radiographic studies, benefits and risks of surgery and detailed discussion with the patient must be completely done. The medical problems in the patient’s history must be evaluated and properly treated. Brain tumor with significant brain edema, must be put on steroid medication. Even when there is no or little edema, if it is thought that there will be lot of brain tissue manipulation at surgery, steroid should be started at least 48 hours prior surgery. Complicating hydrocephalus that may present in certain brain tumors must be considered whether it gives signs and symptoms of raised intracranial pressure. When there is no symptom, nothing needs to be done. Just before the surgery is started, make sure that manitol with a dosage of 1-1.5g/kg has been given and this must be finished within 20-30 minutes. In addition, many surgeons give furosemid with a dosage of 10-20 mg just after the catheter is inserted. Antibiotic is given one hour before surgery and together with steroid are continued at 6 hours intervals. Antiepileptic drug is given when there is a history of seizure attack. The main goals of surgery are to provide specimen for accurate pathological diagnosis and to reduce mass effect. Many factors must be considered in making decision for surgery, including patient’s age, neurological status, general medical condition, degree of mass effect, location of the tumor, extent of abnormality and the patient’s understanding of the risks and benefits of surgery. The success of tumor removal is most likely dependent on thorough imaging studies evaluation, understanding the normal and pathologic anatomy, proper positioning of the patient, well-planned surgical exposure, microsurgical technique familiarity, avoidance of severe and prolong tissue retraction and minimal exposure of normal brain tissue. For benign tumors such as meningioma and neurinoma, complete tumor removal must be considered including excision of affected dura and bone. To avoid severe brain retraction, internal decompression of tumor mass must be first accomplished before removing out the capsule completely. When some part of the tumor strongly attaches to the important structures such as nerves and brain stem, it must be left. If the tumor is malignant such as high grade astrocytoma or glioblastoma, it must be removed out as much as possible while trying to preserve function of eloquent brain area. The surgeon must be aware of the possibility of surgical complications. Majority of complication can be prevented by careful preoperative planning, meticulous technique and familiarity of using microintruments. The surgeon must be intimate with knowledge of the predicted complication. When the patient does not recover promptly, an immediate CT scan must be taken to evaluate the presence of hematoma, brain edema, hydrocephalus, tension pneumocephalus and infarction. The subsequent treatments depend on the result of that scan.

ScenarioA 8 year old boy was presented with 6 months history of gastrointestinal disturbance. He has been brought to medical attention several times, but it seemed to be not help. His school performance was significantly distorted in the last one year. Four weeks before admission he was noted to have difficulty in walking steadily and started to have problem with articulation. On examination revealed bilateral of 6th nerve paralysis, disturbance of all cerebellar function and papil edema. Head CT has been taken and he will be put on surgical tumor removal. The doctor on duty has carefully informed the family



including the aims of surgery, outcomes, postoperative complication, adjuvant modalities following surgery and the possibility of having another surgery for the complication caused by tumor compression.

Learning task1. Describe the possible location of the tumor2. Describe the most likely of the tumor’s histopathology3. Describe the accompanying complication 4. Describe the management of this complication5. Describe the preoperative management6. Describe the surgical approach to exposure this tumor7. Describe the surgical goals of this tumor8. Describe the post operative complications that may appear

Self assessment1. Explain the classification of brain tumors2. Explain the work of manitol in reducing intracranial pressure3. Explain how a brain tumor can cause hydrocephalus 4. Explain how the patient can get bilateral 6th nerve paralysis5. Explain the mechanism of papil edema

DAY 11th

June 9th 2016GULLAIN BARRE SYNDROME AND MYASTENIA GRAFIS


Aim:Describe the patophysiology, epidemiology, clinical presentations, diagnostic work-up,

treatment and prognosis of Guillan-Barre Syndrome (GBS).

Learning outcome:1. Understanding the patophysiology mechanism and the epidemiology of GBS2. Know the clinical presentations of GBS3. Be able to make diagnostic work-up including patient history, clinical finding and another

comprehensive tests (CSF examination, ENMG/NCS)4. Understanding the management of GBS5. Recognize the prognosis of GBS

AbstractGBS is an acute or subacute polyneuropathy that can follow minor infective illnesses,

inoculations, or surgical procedures or may occur without obvious precipitants. Clinical and epidemiologic evidence suggest an association with preceding Campylobacter jejuni infection. Its precise cause is unclear, but it appears to have an immunologic basis. Patients generally present with



weakness that is symmetric, usually begins in leg, is often more marked proximally than distally, and is sometimes so severe that it is life-threatening, especially if the muscles of respiration or swallowing are involved. Sensory complaints while usually less marked than motor symptoms, are also frequent. The deep tendon reflexes are typically absent. There may be marked autonomic dysfunction with tachycardia, labile blood pressure, disturbed sweating, sphincter disturbances and impaired pulmonary function.

The albuminocytological dissociation occur, characterized by increased protein concentration but a normal cell count; abnormalities may not be found in the first week. Electrophysiologic studies may reveal marked slowing of motor and sensory conduction velocity, or evidence of denervation and axonal loss.

Plasmapheresis is best instituted early, indicated especially in patients with a severe or rapidly progressive deficit or respiratory compromise. Intravenous immunoglobulin (400mg/kg/day for 5 days) appears to be equally effective and should be used in preference to plasmapheresis in adults with cardiovascular instability and in children; the two therapies are not additive.

The disorder is self limiting and improvements occurs over the weeks or months following onset. Approximately 70-75% of patients recover completely, 25% are left with mild neurologic deficits and 5% are die, usually as a result of respiratory failure.

Self assessment1. Explain the patophysiology mechanism of GBS!2. Explain the clinical presentation of GBS!3. Describe the diagnostic work-up for GBS!4. Describe the medications approaches and prognosis for GBS!

ScenarioA 20 yrs old man complain weakness of leg muscles, suffered from 2 days ago, ascending type, symmetrical, proximal more pronounced than distal. Previously, two weeks before he felt weakness, he got pronounced diarrhea for 3 days, and it got improved by itself. Leg weakness is not improved by rest. There is no complaint of sensory abnormalities, no micturition or respiratory problem. There is also no history of trauma. From clinical finding there is flaccid paralysis of legs with absent deep tendon reflexes.

Learning task:1. What is the possible diagnosis of this patient?2. What is the diagnostic work up for this patient?3. What condition should we obtain from the CSF examination and what is the interpretation?4. What is the management planned for this patient?

Learning resources:1. Ropper, A., Brown, R. 2009. Adams and Victor’s : Principles of Neurology.

9th ed. New York: McGraw-Hill. p.1405-1414.2. Longmore M, Wilkinson I, Turmezei T, Cheung CK. 2007. Oxford Handbook of Clinical

Medicine. 7th ed. New York: Oxford University Press.

ENSEFALOPATI, KOMAdr. Kumara Tini, Sp.S, FINS



Aim:Describe the definition and pathology of coma, able to work-up and manage the comatose patients.

Learning outcome:1. Describe the definition of coma2. Able to locate the pathology of coma

- A diffuse, bilateral, cortical dysfunction- Damage to ascending reticular activating system (ARAS) located throughout the brainstem

from the medulla to the thalami.3. Able to work-up the comatose patients (History taking, general examination and neurologic

examination)4. Understanding the management of the comatose patients including emergency management.

AbstractComa is a sleeplike state in which the patient makes no purposeful response to the environment

and from which he or she cannot be aroused. Painful stimulation may produce no response or nonpurposeful reflex movements mediated through spinal cord or brainstem pathways. Coma results from a disturbance in the function of either brainstem reticular activating system above the midpons or of both cerebral hemispheres, since these are the brain regions that maintain consciousness.Emergency management of the comatose patient includes the following steps:

1. Ensure patency of the airway and adequacy of ventilation and circulation (ABCs)2. Insert an intravenous catheteter and withdraw blood for laboratory studies (serum glucose and

electrolytes, hepatic and renal function test, prothrombin time, partial thromboplastin time and a complete blood count). Additional studies may be useful in certain cases, such as drug screen.

3. Begin an intravenous infusion and administer dextrose (possible hypoglycemic coma), thiamine (thiamine deficiency patient) and naloxone (possible opiate overdose).

4. Withdraw arterial blood for blood gas and pH determinations5. Institute treatment for seizures, if present. Work-up in comatose patients include history taking , general examination and neurologic

examination. The most crucial aspect of the history is the time over which coma develops, such as a sudden onset of coma suggests a vascular origin; or coma preceded by a confusional state or agitated delirium without lateralizing signs or symptoms, is probably due to a metabolic derangement. General examination must be confined to assessment of repiratory rate and pattern, signs of trauma, blood pressure, temperature, sign of meningeal irritation and optic fundi.

The neurologic examination is the key to etiologic diagnosis in the comatose patient. Document the level of consciousness in objective terms using the Glasgow Coma Scale GCS, a numerical scale for evaluating level of impaired consciousness, that is easily noticed over time and among different examiners. Pupillary size and reactivity, oculocephalic (Doll’s – head maneuver) and oculovestibular (cold - water calorics testing) and the motor response to pain should be evaluated in detail.

The most important step in evaluating and managing the comatose patient is to decide whether unconsciousness is the result of a structural brain lesion or it is secondary to a diffuse encephalopathy caused by metabolic disturbance, meningitis, or seizures. So, the treatment for coma is regarding to the underlying condition, in a structural causes emergency neurosurgical intervention may be critical but in diffuse causes medical treatment may be required. Coma prognosis varies widely depending on underlying causes. Post TBI coma better outcomes than post anoxia coma. Prolonged coma rare, most progress to Persistent Vegetative State within 1 month.



Self assessment1. Explain the definition of coma!2. Explain the pathology of coma!3. Describe the clinical work-up for coma!4. Describe the management of coma!

ScenarioA 9 years old boy admitted to emergency room unconsciously. From general exam there was no history of head trauma, no fever or head stiffness. Hemodynamic with BP 110/70 mmHg, HR:100 bpm, and respiratory distress (RR:28 times/minute, Kussmaul’stype). From neurologic exam, he came with GCS 5, bilateral fixed dilated pupil, and no sign of lateralization. Blood serum showed high glucose value. Blood gas showed compensated metabolic acidosis, with keton found in urine test. Head scan revealed mild cerebral edema.

Learning task:1. What is the possible diagnosis of this patient?2. What is the suspicious pathology mechanism of the unconsciousness state?3. What is the management planned for this patient?

Learning resources:3. Posner, J.B., Saper, C.B., Schiff, N.D., Plum, F., 2007. Plum and Posner’s Diagnosis of Stupor and

Coma. 4th ed. NewYork:Oxford University Press.4. Longmore M, Wilkinson I, Turmezei T, Cheung CK. 2007. Oxford Handbook of Clinical Medicine.

7th ed. New York: Oxford University Press.

DAY 12th

June 10th 2016CENTRAL NERVOUS SYSTEM (CNS) INFECTIONS (1): MENINGITIS,

ENSEFALITIS, MALARIA SEREBRAL, RABIESdr. Ni Made Susilawathi, Sp.S

Aims:Describe diagnosis, initial management and/ or referral patients with CNS infection

Learning Outcome:

1. Differentiate between Meningitis, Encephalitis and brain abscess2. Describe common clinical presentation, Cerebrospinal fluid (CSF) finding and initial management

for the following:a. Bacterial Meningitisb. Viral Meningitisc. Encephalitisd. Brain Abcesse. Cerebral malaria

3. Describe Manifestation HIV infection in Nervous System including:



a. Encephalopathyb. Myelopathyc. Neuropathy

4. Describe opportunistic CNS infection associated with HIV infection5. Explain the patophysiology of CNS infection6. Describe common complication of CNS infection7. Explain the technique meningeal signs patient with CNS infection8. Discuss the need for urgent investigations and referrals

Curriculum Contens:1. History taking patients with CNS infection2. Physical Examination patients with CNS infection3. Initial Management patients with CNS infection

AbstractsInfection can affect the function of the nervous system by damaging the brain (encephalitis,

abscess),its lining (meningitis, subdual empyema), spinal cord (myelitis, cord compression), lumbosacral plexus,muscle and nerves. At least 1% of hospital admission relate to infection of central nervous system (CNS), primarily bacterial meningitis.Encephalitis refers to an acute, usually diffuse inflammatory process affecting the brain. While meningitis is primarily an infection of the meningen,acombined meningoencephalitis my also occur.

Acute bacterial Meningitisis a life-threatening neurological emergency. Early diagnosis and effective antibiotic treatment remains the cornerstone of successful management of ABM. Classic symptoms include headache, fever, neck stiffness and altered mental status. The causative organism of meningitis can be predicted based on the patient’s age, exposure to an epidemic, vaccination against common agents (eg, Haemophilus influenza, Streptococcus pneumonia or Neisseria meningitides) and immune state. The key to diagnosing meningitis lies in examining the cerebrospinal fluid (CSF) by lumbar puncture.

A brain abscess is a focal, suppurative infection within the brai parenchyma, typically surrounded by a vascularized capsule. The term cerebritis is often employed to describe a nonencapsulated brain abscess.

Cerebral malaria is the most severe neurological complication of infection with Plasmodium falciparum malaria. It is a clinical syndrome characterized by coma and asexual forms of the parasite on peripheral blood smears. Mortality is high and some surviving patients sustain brain injury which manifest as long-term neuro-cognitive impairments.

Viral encephalitis is an inflammation of the brain parenchyma caused by a viral vector. Acute or subacute onset of fever, headache and altered mental status are the cardinal features of acute viral encephalitis. Personality change, perceptional disturbance (illusions and hallucinations) and disorientation are common and can heralding symptoms. Herpes simplex virus, arthropod-borne viruses and enteroviruses are the most common causes among adults.

Disease of the CNS is common in HIV infection. Neurologic problem occur throughout the course of disease and may be inflammatory, infectious, demyelinating, or degenerative in nature. These problems fall into four basic categories: neurologic disease caused by HIV itself, HIV related neoplasms, opportunitic infections of the nervous system and adverse effect of medical therapy.

Self Directing LearningBasic knowledge that must be known:

1. The Meningens and The cerebrospinal fluid and ventricular system



2. The technique performing a lumbar puncture/spinal tap3. Cerebrospinal fluid finding in CNS infection

ScenarioA 28 year-old man presents the emergency room with a severe headache, fever and confusion.

He is not known to have any medical illness, and there is no history of head trauma. On examination , he has a temperature of 380C , Blood pressure 110/68 mmHg and pulse 100 beat/min. His neurologic examination is notable for kernig sign and hyperreflexia. Learning Task:

1. What is the most likely diagnosis ?2. What is the best diagnostic next step ?3. What is the next step on theraphy ?4. What is the differential diagnosis of this patient?

Self Assessment 1. Know the clinical presentation of meningitis and encephalitis2. Learn to develop a diagnostic strategy for the diagnosis of meningitis and encephalitis and

understand the cerebrospinal fluid finding in bacterial, tuberculosis and viral3. Know strategy for meningitis in the emergency room

~ CURRICULUM MAP ~Smstr Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerkship

7

Medical Emergency(3 weeks)BCS (1 weeks)

Special Topic:-Travel medicine(2 weeks)

Elective Study III(6 weeks)

Clinic Orientation (Clerkship)(6 weeks)

6

The Respiratory System and Disorders(4 weeks)BCS (1 weeks)

The Cardiovascular System and Disorders(4 weeks)BCS (1 weeks)

The Urinary System and Disorders(3 weeks)

BCS (1 weeks)

The Reproductive System and Disorders (3 weeks)

BCS (1 weeks)

5Elective Study II(1 weeks)

Alimentary & hepato-biliary systems& disorders

The Endocrine System, Metabolism and Disorders(4 weeks)

Clinical Nutrition and Disorders(2 weeks)

Special Topic : - Palliative medicine-Compleme

Elective Study II(1 weeks)



(4 Weeks)

BCS (1 weeks)BCS (1 weeks)

BCS (1 weeks) ntary & Alternative Medicine - Forensic(3 weeks)

4

Musculoskeletal system &connectivetissue disorders(4 weeks)

BCS (1 weeks)

Neuroscienceandneurologicaldisorders(4 weeks)

BCS (1 weeks)

Behavior Changeand disorders(4 weeks)

BCS(1 weeks)

The Visualsystem &disorders(2 weeks)

BCS(1 weeks)

3

Hematologicsystem & disor-ders & clinical oncology(4 weeks)

BCS (1 weeks)

Immune system &disorders(2 weeks)

BCS(1 weeks)

Infection & infectiousdiseases(5 weeks)

BCS (1 weeks)

The skin & hearing system& disorders(3 weeks)

BCS(1 weeks)

2

Medical Professionalism(2 weeks)

BCS (1 weeks)

Evidence-based Medical Practice(2 weeks)

Health System-based Practice(3 weeks)

BCS (1 weeks)

Community-based practice(4 weeks)

Special Topic- Ergonomi- Geriatri(2 weeks)

Elective Study I(2 weeks)

1

StudiumGenerale and Humaniora(3 weeks)

Medicalcommunication(3 weeks)

BCS (1 weeks)

The cellas bioche-mical machinery(3 weeks)

BCS(1 weeks)

Growth&development(4 weeks)

BCS: (1 weeks)

Pendidikan Pancasila & Kewarganegaraan (3 weeks)


fk.unud.ac.id · web viewkomponen susunan saraf pusat terdiri dari otak (ensefalon, yang...

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