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.
~ 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 (3rdfloor)
1 dr. I Gede Putu Supadmanaba, S.Ked 1 Biochemistry 082146558748 3R.3.09rd floor:
2 Ni Putu Wardani, Sp.An, M.Biomed 2 DME 081337660988 3R.3.10rd floor:
3 dr. Putu Ariastuti, MPH 3 Public Health 0818560008 3R.3.11rd floor:
4 dr. Ida Bagus Sutha, Sp.P-K 4 Pulmonology 08123990362 3R.3.12rd floor:
5 dr. Muliani, M.Biomed 5 Anatomy 085103043575 3R.3.13rd floor:
6 dr. Ni Made Ari Suryathi, M.Biomed, Sp.M 6 Opthalmology 085253651928 3R.3.14rd floor:
7 dr.Ni Luh Putu Ratih Vibriyanti Karna,Sp.KK 7 Dermatology 081337808844 3R.3.15rd floor:
8 dr. Putu Gede Sudira, Sp.S 8 DME 081805633997 3R.3.16rd floor:
9 dr. Agung Nova Mahendra, M.Sc 9 Pharmacology 087861030195 3R.3.17rd floor:
10 dr. Ari Andayani, Sp.M 10 Opthalmology 08113803666 3R.3.19rd floor:
English Class (Class B)
No Name Group Departement Phone (3Venuerdfloor)
1 dr. I G N Wien Aryana, Sp.OT 1 Orthopaedi 0811385263 3R.3.09rd floor:
2 Prof.dr. I Dw Pt Sutjana, PFK, M.Erg 2 Fisiology 08123924477 3R.3.10rd floor:
3 dr. Ida Ayu Kusuma Wardani, Sp.KJ, MARS 3 Psychiatry 08123813831 3R.3.11rd floor:
4 Dr.rer.Nat. dr. Ni Nyoman Ayu Dewi, M.Si 4 Biochemistry 081337141506 3R.3.12rd floor:
5 Dr.dr. I Made Muliarta, M.Kes 5 Fisiology 081338505350 3R.3.13rd floor:
6 dr. I G P Suka Aryana, Sp.PD-Kger-FINASIM 6 Interna 08164724600 3R.3.14rd floor:
7 Dr. dr. Made Sudarmaja, M.Kes 7 Parasitology 08123953945 3R.3.15rd floor:
8 Dr.dr. Ni Nyoman Sri Budayanti, Sp.MK(K) 8 Microbiology 08553711398 3R.3.16rd floor:
9 dr. I Wayan Sugiritama, M.Kes 9 Histology 08164732743 3R.3.17rd floor:
Neuroscience Basic Semester IV
Topic and Schedule Reguar and English Class Day/Dat
e
Activity Class B Class A Venues Conveyer
1
May 19th
LEARNING PROGRAM
Day 1
stBagian Anatomi FK UNUD
ABSTRAKSetiap 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: 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.
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
ndBagian 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
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
rdBagian 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
thNEUROPHYSIOLOGY
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
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
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.
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
thNEUROPHYSIOLOGY
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
DAY 6
thHistology
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 !
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
5. CNS Infection
6. Demyelinating disease
7. Degenerative disease of CNS 8. Tumors of CNS
DAY 7
thClinical 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.
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
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 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
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
Clinical Neuroscience Semester IV Topic and Schedule English Class
Date Topic/Module Class B Venues Conveyer
1
dr. Ketut Widiastuti , Sp.S dr. Made Wiranadha Sp.THTKL
dr. Dewi Sutriani Maharini, Sp.A
Dr. dr. Anna Marita, Sp.S(K)
Facilitators.
3
dr. Made Oka Adnyana, Sp.S(K) dr. Made Widhiasih, SpRad
Facilitators.
dr. Made Oka Adnyana, Sp.S(K)/ dr. Made Widhiasih, SpRad
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
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
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,
Dr.dr. DPG. Purwa Samatra, Sp.S(K)
Facilitators.
dr. Widiasttuti, Sp.S/ Dr.dr. DPG. Purwa Samatra, Sp.S(K)
Prof. Dr. dr. Sri Maliawan, SpBS(K)
SGD
dr. IA. Sri Wijayanti, Sp.S/ Prof. Dr. dr. Sri Maliawan, SpBS(K)
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
Dr.dr. Tjokorda GB. Mahadewa, M.Kes., SpBS(K)Spinal
Dr.dr. Made Golden , Sp.BS (K)
2016 GBS, Myastenia
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
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
dr. I.A Sri Wijayanti, M.Biomed, Sp.S
dr. Ketut Widyastuti, Sp.S
June 17th
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
dr. Ketut Widiastuti , Sp.S dr. Made Wiranadha Sp.THTKL
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
dr. Made Oka Adnyana, Sp.S(K)/ dr. Made Widhiasih, SpRad
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
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
2016
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
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)
Prof. Dr. dr. Sri Maliawan, SpBS(K)
Prof. Dr. dr. Sri Maliawan, SpBS(K)
Facilitators.
9
dr. Wayan Niryana, M.Kes, SpBS(K)
Facilitators.
dr. AABN.Nuartha,Sp.S(K)/ dr. Wayan Niryana, M.Kes, SpBS (K)
10
Dr.dr. Made Golden, Sp.BS (K)
Facilitators.
Dr.dr. Tjokorda . Mahadewa, M.Kes., SpBS(K)Spinal / Dr.dr. Made Golden SP.BS(K)
dr. Kumara Tini, Sp.S, FINS
Facilitators.
Plenary 14.00-15.00 Class room dr. Kumara Tini, Sp.S, FINS
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 26th2016.
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
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
Learning outcome: Can describe the:
1. Diagnosis of meniere disease
2. Differential Diagnosis of meniere disease 3. Management for meniere disease
4. Prognosis of meniere disease 5. Further investigations and referrals
Curriculum contens:
1. History taking of meniere disease
2. Physical Examination of meniere disease
3. Investigation routine and specific of meniere disease 4. Management for meniere disease
Abstracts
Meniere disease also called endolymphatic hydrops, is a disorder that can affect hearing and balance
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..
Scenario
A 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 PALSY Aims:
Describe diagnosis, management and/ or referral patients with facial palsy
Learning outcome: Can describe the:
2. Differential Diagnosis of Bell’s Palsy 3. Management for Bell’s Palsy
4. Prognosis of Bell’s Palsy
5. Further investigations and referrals
Curriculum contens:
1. History taking of Bell’s Palsy
2. Physical Examination of facial palsy patients 3. Investigation routine and specific of Bell’s Palsy 4. Management for Bell’s Palsy
Abstracts
Bell’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 learning
Basic knowledge that must be known: 1. The anatomy of Facial nerve 2. Facial Palsy
3. Bell’s Palsy
4. Factors that affect Bell’s Palsy
Scenario
A 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 assessment
1. 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?
1. PERDOSSI. Pedoman dan Tatalaksana Vertigo 2012 2. Adam and Victor’s. Principles of Neurology 8th. 3. Wikipedia. Meniere Disease
HEARING LOSS
dr. Made Wiranadha, Sp. THT-KL Abstract
There 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 assessment
Learning 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 Objective CASE 1
A 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 Task
1. 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?
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?
From
Menner, A Pocket Guide to the Ear © 2003 Thieme
DAY 2nd
May 27th 2016
FEBRILE SEIZURE IN CHILDREN dr. 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 seizure
3. Risk factors of recurrent febrile seizure and genetic epilepsy with febrile seizures plus (GEFS+) 4. Immediate medical management of acute seizure and status epilepticus
5. Long term management for prevention of recurrent febrile seizure (intermittent and long term prophylaxis)
Abstract of Lecture
Febrile 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.
