Study Guide Neuroscience Semester IV 16 Mei 2016

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.

~ 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

FACILITATORS ~ Regular Class (Class A)

No Name Group Departement Phone

Venue (3rd_floor)

1 dr. I Gede Putu Supadmanaba, S.Ked 1 Biochemistry 082146558748 3_R.3.09rd floor: 2 Ni Putu Wardani, Sp.An, M.Biomed 2 DME 081337660988 3_R.3.10rd floor: 3 dr. Putu Ariastuti, MPH 3 Public Health 0818560008 3_R.3.11rd floor: 4 dr. Ida Bagus Sutha, Sp.P-K 4 Pulmonology 08123990362 3_R.3.12rd floor: 5 dr. Muliani, M.Biomed 5 Anatomy 085103043575 3_R.3.13rd floor: 6 dr. Ni Made Ari Suryathi, M.Biomed, Sp.M 6 Opthalmology 085253651928 3_R.3.14rd floor: 7 dr.Ni Luh Putu Ratih Vibriyanti Karna,Sp.KK 7 Dermatology 081337808844 3_R.3.15rd floor: 8 dr. Putu Gede Sudira, Sp.S 8 DME 081805633997 3_R.3.16rd floor: 9 dr. Agung Nova Mahendra, M.Sc 9 Pharmacology 087861030195 3_R.3.17rd floor: 10 dr. Ari Andayani, Sp.M 10 Opthalmology 08113803666 3_R.3.19rd floor: English Class (Class B)

No Name Group Departement Phone ₍₃Venuerd_floor)

1 dr. I G N Wien Aryana, Sp.OT 1 Orthopaedi 0811385263 3_R.3.09rd floor: 2 Prof.dr. I Dw Pt Sutjana, PFK, M.Erg 2 Fisiology 08123924477 3_R.3.10rd floor: 3 dr. Ida Ayu Kusuma Wardani, Sp.KJ, MARS 3 Psychiatry 08123813831 3_R.3.11rd floor: 4 Dr.rer.Nat. dr. Ni Nyoman Ayu Dewi, M.Si 4 Biochemistry 081337141506 3_R.3.12rd floor: 5 Dr.dr. I Made Muliarta, M.Kes 5 Fisiology 081338505350 3_R.3.13rd floor: 6 dr. I G P Suka Aryana, Sp.PD-Kger-_FINASIM 6 Interna 08164724600 3_R.3.14rd floor: 7 Dr. dr. Made Sudarmaja, M.Kes 7 Parasitology 08123953945 3_R.3.15rd floor: 8 Dr.dr. Ni Nyoman Sri Budayanti, Sp.MK(K) 8 Microbiology 08553711398 3_R.3.16rd floor: 9 dr. I Wayan Sugiritama, M.Kes 9 Histology 08164732743 3_R.3.17rd floor: 10 dr. I Made Susila Utama, Sp.PD-KPTI 10 Interna 08123815025 3_R.3.19rd floor:

Neuroscience Basic Semester IV

Topic and Schedule Reguar and English Class Day/Dat

e

Activity Class B Class A Venues Conveyer

1 May 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. Mangku 2

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. Muliani 3

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. Mangku

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 5

May 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. Inten 6

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 7

May 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 8

May 25th 2016

Evaluation 09.00-11.00 09.00-11.00 Class room LECTURER, FACILITATORS.

LEARNING PROGRAM

Day 1

st

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 spinalis

2. 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 Kuliah

1. 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 cerebrospinalis

Subtopik: meninges, vaskularisasi SSP, sirkulasi liquor cerebrospinalis, garis besar pertumbuhan dan perkembangan SSP.

Learning objective Topik Kuliah 1: Refleks Segmental, intersegmental dan suprasegmental 1. Menjelaskan anatomi fungsional system saraf secara umum

2. Mengggambarkan berbagai bentuk sel saraf dan bagian-bagiannya 3. Menjelaskan jenis sel saraf berdasarkan sifatnya

4. Menjelaskan sifat axon, selubung myelin dan mekanisme pengantaran gelombang depolarisasi dan repolarisasi

5. 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 umum 7. Menjelaskan komponen utama suatu lengkung reflex yang paling sederhana 8. 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 SSP 12. Menjelaskan anatomi nervi spinals dan nervi craniales beserta sifat-sifatnya

13. 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-sifatnya 4. Jelaskan anatomi dan fungsional nervi craniales

5. 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. ABSTRACT

Every 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:

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 cerebrospinalis

Subtopic: meninges, CNS vascularization, the circulation of liquor cerebrospinalis, outline growth and development of the CNS.

Learning objective Lecture Topic 1: Segmental reflex, intersegmental and suprasegmental 1. Describe the functional anatomy of the nervous system in general

2. Draw various forms of nerve cell and its parts 3. Describe the types of nerve cells by their nature

4. Explain the nature of axons, the myelin sheath and delivery mechanisms wave of depolarization and repolarization

5. Understand the type of synapse, neurotransmitters and other types of delivery mechanisms impulses through synapses area

6. Distinguish CNS and PNS in terms of location, function and common histological composition 7. 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 properties

12. 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 synapses

3. Draw a chart of spinal nerves, components and its properties 4. Explain the anatomical and functional aspect of nervi craniales

5. 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.

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 2

nd

Bagian Anatomi FK UNUD

Learning Objective Topik Kuliah 2: Koordinasi pergerakan dan keseimbangan

1. Menjelaskan peran batang otak dalam menghantarkan impuls motorik dan sensorik 2. Menjelaskan struktur, peran dan fungsi formatio reticularis

3. Menjelaskan arsitektur struktur cerebellum dan hubungan aferen dan eferen dengan nuclei di luar cerebellum

4. 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 spinalis

6. Menjelaskan pusat-pusat yang berkaitan dengan emosi 7. Menjelaskan jalur saraf yang mengendalikan keseimbangan 8. 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 dalamnya 2. Jelaskan jalur saraf motorik dari cortex cerebri sampai ke saraf cranial dan spinal 3. Jelaskan peran ganglia basalia dalam koordinasi pergerakan

4. Jelaskan anatomi susunan saraf pyramidal dan extrapyramidal serta konsekuensi dan kerusakan kedua system ini

5. Jelaskan pusat-pusat neuron yang mengatur emosi Kasus 2

Sesudah 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 dalamnya

2. Jelaskan hubungan-hubungan cerebelulum dengan nuclei extra cerebellar dalam pengaturan pergerakan dan keseimbangan

3. 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 pendengaran 5. Jelaskan perjalanan saraf pembau sampai ke pusat pembauan.

Learning objective Lecture Topic 2: Coordination of movement and balance 1. Explain the role of the brain stem in delivering sensory and motor impulses 2. Describe the structure, role and functions of formatio reticularis

3. 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 cord

6. Explain the centers related to emotions

7. Describe the neural pathways that control balance

8. 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 it

2. Explain the motor nerve pathways from the cerebral cortex to the cranial and spinal nerves 3. Describe the role ganglia basalia in coordinating the movement

4. Explain the anatomy of the pyramidal and extrapyramidal nervous system as well as the consequences and damage to both this system

5. Describe the centers of neurons that regulate emotion Case 2

After 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 balance

3. 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 3

rd

Bagian Anatomi FK UNUD

1. 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 SST 3. Menjelaskan regionalisasi vaskularisasi otak.

4. Menjelaskan sirkulasi liquor cerbri

5. Menjelaskan garis besar pertumbuhan dan perkembangan SSP 6. Menjelaskan kelainan congenital SSP.

Kasus 1

Seorang 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 meninges

3. Jelaskan hubungan antar ruang tersebut

4. Jelaskan perjalanan aliran liquor serebrospinalis

5. Jelaskan hubungan liquor serebrospinalis dengan pembuluih darah Kasus 2

Seorang 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 SSP

2. Jelaskan tentang Circulus Arterosus Cerebri (Willis). pembuluh darah yang melayani otak dan daerah layanannya

3. 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 PNS 2. Explain the regionalization vascularisation of the brain. 3. Explain the circulation of liquor cerbri

4. Explain the outline of growth and development of the SSP 5. 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 CNS 2. Name of the space between the layers of the meninges

3. Describe the relationship between space 4. Explain the trip flow of cerebrospinal liquor

Case 2

A 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 CAN 2. Tell about Circulus Arterosus Cerebri (Willis).

3. Describe blood vessels serving the brain and its service area 4. Describe and explain diagrams that serve the spinal cord arteriae 5. Describe the occurrence of hydrocephalus and spina bifida.

Day 4

th

NEUROPHYSIOLOGY

dr. 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 receptors 3. Motor division – the effectors

4. Processing of information – memory 5. Memory storage

II. MAJOR LEVEL OF THE CNS 1. Cortical level

2. Subcortical level 3. Spinal cord level

III. CENTRAL NERVOUS SYSTEM SYNAPSES 1. Types of synapses

2. Physiologic anatomy of the synapses

3. Chemical substances that function at synaptic transmission 4. Electrical events during neuronal excitation and inhibition 5. Special function of dendrites in exciting neurons

6. Relation of state of excitation - the neuron to rate of firing 7. Some special characteristics of synaptic transmission. ABSTRACT

I. 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 differ

5. 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 potential 10. Explain the synaptic transmission exhibits special characteristic

11. 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 study

a) 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 intact

1. What is the reason for the loss of the motor function without loss of pain sensation is that in the nerves to his arm

2. What is a thorough general physical examination should be made in this case. 3. Which one of the sensory test should be done

4. Which one of the reflex test should be done

5. Describe general physical examination should always be done in motor system of this case

b) 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 sclerosis

1. 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 5

th

NEUROPHYSIOLOGY

dr. 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 QUESTION

1. 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 force

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

4. Define reciprocal innervation, inverse stretch reflex, clonus and lengthening reaction 5. Describe in general terms how posture and movement are regulated

6. Discuss the function of the cerebral cortex, cerebellum, basal ganglia, and corticospinal and corticobulbar tracts in skilled voluntary movement

7. 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 study

a) 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 6

th

Histology

HISTOLOGICAL 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 3

A 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-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 cerebellum

9. 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!

NEUROPATHOLOGY

Dr. Ni Putu Sriwidyani, Sp.PA

ABSTRACT

The 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 TASK Case 1

A 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 performed

3. What is the possible diagnosis of this tumor. Case 2

A 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 3

A 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 ASSESMENT

Describe and give some example of:

1. Cerebral edema, hydrocephalus, and raised intracranial pressure. 2. Malformation and developmental disease

3. Trauma affecting CNS 4. Cerebrovascular disease

5. CNS Infection

6. Demyelinating disease

7. Degenerative disease of CNS 8. Tumors of CNS

DAY 7

th

Clinical Pathology

Dr. 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?

PHARMACOLOGY

Dr. dr. I Made Jawi, M.Kes

DRUGS USED FOR SEIZURE DISORDERS

AIMS :

1. Describe the rationale drugs used to treat each type of seizure 2. Describe the desired therapeutics outcomes for seizure disorders 3. Develop a education plan for people diagnosed with a seizure disorder LEARNING OUTCOMES :

Apply concepts and principles of drugs used for seizure CURRICULUM CONTENT

1. 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 ABSTRACT

Seizures 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.

SCENARIO

Mr 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 ASSESMENT

1. 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 disease 2. Describe the desired theraupetic outcomes for parkinson’s disease 3. 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 CONTENT

Drug therapy for Parkinson’s Disease - Drug class : Dopamine Agonists - Drug class : COMT Inhibitor

- Drug class : Anti cholinergic Agents

- Drug Class : Miscellaneous Anti parkinsonism Agents ABSTRACT

Parkinson’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 TASK

1. 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 symptoms

4. 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 ASSESMENT

1. Describe the rationale drugs used to treat parkinson’s disease 2. Describe the side effect of drugs that used for parkinson’s diseas

3. Develop an education plan for people diagnosed with parkinson’s disease

TOPIK STUDENT PROJECT

Regular Class (Class A)

Group

SGD Judul Student project Pembimbing Evaluator

1 BPPV Facilitator dr. Kt. Widiastuti, Sp.S

2 Lesi Batang Otak Facilitator dr. Kt. Widiastuti, Sp.S 3 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. Rad 8 Neurogenic bladder Facilitator Dr. Kumara Tini, Sp.S , FINS 9 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)

Group

SGD Judul Student project PEMBIMBING EVALUATOR

1 Afasia Facilitator dr. Kt Widiastuti, SP.S

2 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.S

7 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 IV Topic and Schedule English Class

Date Topic/Module Class B Venues Conveyer

1 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.S dr. Made Wiranadha Sp.THTKL 2

May 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).

3 May 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 4

May 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 5

June 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, Biomed Dr. dr. Pt. Pramana, Sp.

Sp.BS(K) spinal 6

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

7 June 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)

8 June 6th

2016

Student project CNS Tumor primer dan sekunder

Traumatic Brain Injury, hematom epidural, hematom subdural. Neurofuncional surgery 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)

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)

9 June 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) 10

June 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)

11 June 9th

2016 GBS, Myastenia Grafis Ensefalopati, Koma Break IL/Self Ass SGD Plenary 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), SP.S

dr. Kumara Tini, Sp.S, FINS

Facilitators.

Prof. Dr.dr. Raka Sudewi, Sp.S (K)/ dr. Kumara Tini, Sp.S, FINS 12

June 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/Dat

e

Activity Class B Venue Conveyor

June 13th 2016 June 14th 2016 June 15th 2016 June 16th 2016

Presentasi Student project

Basic clinical skill Motorik, koordinasi, sensorik

Basic clinical skill Fungsi luhur dan refleks

Basic clinical skill Fungsi saraf kranial, Tulang belakang dan meningeal sign, tanda ischialgia 10.00-12.00 11.00-13.00 11.00-13.00 11.00-13.00 Ruang sidang lt.IV Skill Lab Skill Lab Skill Lab Semua Lecturer

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

dr. Ketut Widyastuti, Sp.S

June 17th 2016

Basic clinical skill Pemeriksaan Diagnostik Radiologi dan elektrodiagnostik

11.00-13.00 Skill Lab dr. Kumara Tini, Sp.S, FINS

June 20th

2016 EVALUATION 08.30-10.30

Clinical Neuroscience Semester IV Topic and Schedule Regular Class

Date Topic/Module Class A Venues Conveyer

1 May 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.S dr. Made Wiranadha Sp.THTKL 2

May 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 Tension Headache

and Cluster Headache

May 30th

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 4

May 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 5

June 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

6 June 2nd

CTS, TTS, peroneal palsy

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

2016

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

7 June 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)

8 June 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

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

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

Facilitators.

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

9 June 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) 10

June 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)

11 June 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

dr. Kumara Tini, Sp.S, FINS

Facilitators.

Plenary 14.00-15.00 Class room dr. Kumara Tini, Sp.S, FINS 12

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

dr. Susilawathi, Sp.S

dr. Susilawathi, Sp.S

Facilitators.

dr. Susilawathi, Sp.S June 13th

2016 June 14th 2016 June 15th 2016 June 16th 2016

June 17th 2016

Presentasi Student project

Basic clinical skill Motorik, koordinasi, sensorik

Basic clinical skill Fungsi luhur dan refleks

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

Basic clinical skill Pemeriksaan Diagnostik Radiologi 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. Ketut Widyastuti, Sp.S

dr. Ni Made Susilawathi, Sp.S

dr. Kumara Tini, Sp.S, FINS

June 20th

LEARNING PROGRAM CLINICAL NEUROSCIENCE DAY 1st

May 26th_2016.

VERTIGO, MENIERE DISEASE AND BELL’S PALSY dr. Ketut Widyastuti, Sp.S

Aims:

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

Can describe the: 1. Type of dizziness

2. Differentiation between peripheral vestibular vertigo and central vestibular vertigo 3. Differentiation between vestibular vertigo and non vestibular vertigo

4. Examinations of dizzy patients

5. Initial management principle for vertigo

6. Evaluation the need for urgent investigations and referrals Curriculum contens:

1. History taking of Dizziness

2. Physical Examination of dizzy patients 3. Investigation routine and specific of vertigo 4. Initial Management for vertigo

Abstracts

Vertigo 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 learning

Basic knowledge that must be known:

1. The Equilibrium System and The Vestibular System 2. Peripheral vestibular vertigo

3. Central vestibular vertigo 4. Non vestibular vertigo Scenario

A 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

1. Understanding the patophysiology mechanism and the epidemiology of GBS 2. Know the clinical presentations of GBS

3. 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 GBS 5. Recognize the prognosis of GBS

Abstract

GBS 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 assessment

1. 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!

Scenario

A 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?

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, KOMA

dr. 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 coma 2. 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.

Abstract

Coma 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 determinations

5. 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 assessment

1. 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!

Scenario

A 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 ₂₀₁₆

CENTRAL NERVOUS SYSTEM (CNS) INFECTIONS (1): MENINGITIS, ENSEFALITIS, MALARIA SEREBRAL, RABIES

dr. Ni Made Susilawathi, Sp.S

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

Learning Outcome:

1. Differentiate between Meningitis, Encephalitis and brain abscess

2. Describe common clinical presentation, Cerebrospinal fluid (CSF) finding and initial management for the following:

a. Bacterial Meningitis b. Viral Meningitis c. Encephalitis d. Brain Abcess e. Cerebral malaria

3. Describe Manifestation HIV infection in Nervous System including: a. Encephalopathy

b. Myelopathy c. Neuropathy

4. Describe opportunistic CNS infection associated with HIV infection 5. Explain the patophysiology of CNS infection

6. Describe common complication of CNS infection

7. Explain the technique meningeal signs patient with CNS infection 8. Discuss the need for urgent investigations and referrals

Curriculum Contens:

1. History taking patients with CNS infection

2. Physical Examination patients with CNS infection 3. Initial Management patients with CNS infection

Abstracts

Infection 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 Learning

Basic knowledge that must be known:

1. The Meningens and The cerebrospinal fluid and ventricular system 2. The technique performing a lumbar puncture/spinal tap

3. Cerebrospinal fluid finding in CNS infection

Scenario

A 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 380_{C , 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 encephalitis

2. Learn to develop a diagnostic strategy for the diagnosis of meningitis and encephalitis and understand the cerebrospinal fluid finding in bacterial, tuberculosis and viral

3. Know strategy for meningitis in the emergency room

~ CURRICULUM MAP ~

Smstr

Program or curriculum blocks

10 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)

5

Elective Study II (1 weeks) Alimentary & hepato-biliary systems & disorders (4 Weeks) BCS (1 weeks)

The Endocrine System, Metabolism and Disorders (4 weeks) BCS (1 weeks)

Clinical Nutrition and Disorders

(2 weeks) BCS (1 weeks)

Special Topic : - Palliative medicine -Compleme ntary & Alternative Medicine - Forensic (3 weeks) Elective Study II (1 weeks) 4 Musculoskeletal system & connective tissue disorders (4 weeks) BCS (1 weeks)

Neuroscience and

neurological disorders (4 weeks) BCS (1 weeks)

Behavior Change and disorders (4 weeks) BCS(1 weeks) The Visual system & disorders (2 weeks) BCS (1 weeks) 3 Hematologic system & disor-ders & clinical oncology (4 weeks) BCS (1 weeks)

Immune system & disorders (2 weeks) BCS(1 weeks) Infection & infectious diseases (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 Studium Generale and Humaniora (3 weeks) Medical communication (3 weeks) BCS (1 weeks)

The cell as bioche-mical machinery (3 weeks) BCS(1 weeks) Growth & development (4 weeks) BCS: (1 weeks) Pendidikan Pancasila & Kewarganegaraan (3 weeks)