fk.unud.ac.id · Web viewThe diabete is not controll carefully. Three days ago he had strok affected on branches of vertebral artery: left posterior inferior cerebellar artery and

Study Guide Neuroscience and Neurological Disorders

The seven general core competency

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

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

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

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

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

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

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

Faculty of Medicine Udayana University, DME 1


~ LECTURERS ~

NO NAME DEPARTMENT PHONE

1 dr. Wayan Suarya, PAK. Anatomy 08173552472 dr. I Ketut Karna, AIF., M.Kes. Fisiology 081238141043 dr. I Wayan Sugiritama, M.Kes. Histology 081647327434 Dr. dr. I Made Jawi, M.Kes Pharmacology 081797879725 dr. Ida Bagus Ngurah, M.For. Pharmacology 081236872886 dr. A.A.B.N. Nuartha, SpS(K) Neurology 081797822407 Dr. dr. DPG. Purwa Samatra, SpS(K) Neurology 081239187318 dr. I Made Oka Adnyana, SpS(K) Neurology 08173476979 dr. IGN. Budiarsa, SpS Neurology 0811399673

10 dr. IGN. Purna Putra, SpS(K). Neurology 0812391576311 Dr.dr.AAP laksmi Dewi, Sp.S(K) Neurology 081138881814 dr. Desak Ketut Indrasari Utami, SpS. Neurology 081138509915 dr. I Putu Eka Widyadharma, M.Sc., SpS(K) Neurology 08132804936016 dr. Kumara Tini, Sp.S, FINS Neurology 08123870108117 dr. I.A. Sri Wijayanti, M.Biomed, Sp.S Neurology 08133766793918 dr. Made Susilawathy, Sp.S Neurology 0812469013719 dr. Dewi Sutriani Maharini, Sp.A Pediatric 0812364146620 Prof. DR. dr. Sri Maliawan, SpBS(K) Neuro Surgery 081139846622 Dr. dr. Tjok. Gd. Bagus Mahadewa, M.Kes.,

SpBS(K) SpinalNeuro Surgery 0818484654

23 dr. Wayan Niryana, SpBS(K) Neuro Surgery 0817920195824 dr. Made Wiranadha, Sp. THT-KL Otorhinolaryngology 08123968294

25 Dr.dr. Putu Pramana Suarjaya, SpAn., M.Kes. Anasthesi 081139481126 dr. Widhiasih, Sp.RAD Radiology 08191644262627 dr. Ni Putu Sriwidnyani, SpPA Anatomy Phatology 08133711501228 dr. I Nyoman Wande, SpPK Clinical Phatology 08128768555

29 dr. Muliani, M.Biomed Anatomy 085103043575



~ FACILITATORS ~

Regular Class (Class A)

No Name Group Departement Phone Venue(3rd floor)

1 dr. Ni Made Renny Anggreni Rena , Sp.PD A1 Interna 081803651656 3nd floor: R.3.01

2 dr. I Made Krisna Dinata, S.Ked A2 Fisiology 08174742566 3nd floor: R.3.02

3 dr. I Made Dwijaputra Ayustha, Sp.Rad A3 Radiology 08123670196 3nd floor: R.3.03

4 dr. I Made Bagiada, Sp.PD A4 Interna 08123607874 3nd floor: R.3.04

5 dr. I Made Agus Kresna Sucandra, Sp.An A5 Anasthesi 08123621422 3nd floor: R.3.05

6 dr. I Ketut Wibawa Nada, Sp.An A6 Anasthesi 08123650164 3nd floor: R.3.06

7 dr. I Ketut Suanda, Sp.THT-KL A7 ENT 081337788377 3nd floor: R.3.07

8 dr. I Made Pande Dwipayana, Sp.PD A8 Interna 08123657130 3nd floor: R.3.08

9 dr I Gusti Ayu Dewi Ratnayanti, M.Biomed A9 Histology 087761499889 3nd floor: R.3.20

10 dr. I Gusti Ngurah Mahaalit Aribawa , Sp.An A10 Anasthesi 0811396811 3nd floor: R.3.21

11 dr. I Gde Haryo Ganesha, S.Ked A11 DME 081805391039 3nd floor: R.3.22

12 dr. Ni Wayan Winarti , Sp.PA A12Anatomy Pathology 087860990701 3nd floor:

R.3.23

English Class (Class B)

No Name Group Departement Phone Venue(3rd floor)

1 dr. I Gusti Nyoman Darma Putra , Sp.KK B1 Dermatology 08124644451 3nd floor: R.3.01

2dr. I Gusti Ayu Sri Mahendra Dewi, Sp.PA(K) B2

Anatomy Pathology 081338736481 3nd floor:

R.3.02

3 dr. I Gusti Ayu Sri Darmayani, Sp.OG B3 DME 081338644411 3nd floor: R.3.03

4dr. I Gusti Ayu Putu Eka Pratiwi, M.Kes.,Sp.A B4 Pediatric

08123920750 3nd floor: R.3.04

5 dr. Made Agus Dwianthara Sueta, Sp.B B5 Surgery 081338648424 3nd floor: R.3.05

6 dr. I Putu Eka Widyadharma, MSc,SpS B6 Neurology 081328049360 3nd floor: R.3.06

7 dr. I Gst.Ngr.Ketut Budiarsa , Sp.S B7 Neurology 0811399673 3nd floor: R.3.07

8 dr. I Gede Ketut Sajinadiyasa, Sp.PD B8 Interna 081237068670 3nd floor:



R.3.08

9 dr. I Wayan Juli Sumadi, Sp.PA B9Anatomy Pathology 082237407778 3nd floor:

R.3.20

10 dr. I Made Muliarta, M.Kes B10 Fisiology 081338505350 3nd floor: R.3.21

11 dr. Ni Made Linawati,M.Si B11 Histology 081337222567 3nd floor: R.3.22

12 dr. I B. Putrawan, Sp.PD B12 Interna 081236194672 3nd floor: R.3.23



Basic Neuroscience Semester IVTopic and Schedule Regular and English Class

Day/Date Activity Class B Class A Venues Conveyer

1March 27th

2015

Introduction lecture.Individual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.0009.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.0012.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room-

Discussion room

--

Class room

dr. K. Karna.

Facilitators

dr. K. Karna.

2March 30th

2015

LectureIndividual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.0009.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.0012.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room-

Discussion room

--

Class room

dr. K. Karna

Facilitators

dr. K. Karna

3March 31th

2015

Lecture: Nervous system: neuron, synapsis, medulla spinalis, nn cranialis, brain stem.Individual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.00

12.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room

-Discussion

room--

Class room

dr. Suarya

Facilitators

dr. Suarya

4April 1st

2015

Lecture formation reticularis, cerebellum, telencehalon.Individual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.00

12.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room-

Discussion room

-Class room

dr. Suarya

Facilitators

dr. Suarya5

April 2nd

2015

Lecture diencephalon, ganglia basalia, saraf pembau, meningen, liquor, vascularisasi SSPIndividual LearningSGD

08.00-09.00

09.00-10.3010.30-12.00

09.00-10.00

12.00-13.3013.30-15.00

Class room

-Discussion

dr. Suarya

Facilitators



BreakSP/Self AssessmentPlenary

12.00-12.3012.30-14.0014.00-15.00

11.30-12.0010.00-11.3015.00-16.00

room-

Class roomdr. Suarya

6April 6th

2015

Lecture

Individual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.00

12.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room

-Discussion

room-

Class room

Histology/Pathology Anatomy

HistologyPathology Anat

7April 7th

2015

Lecture

Individual LearningSGDBreakSP/Self AssessmentPlenary

08.00-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-10.00

12.00-13.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room

-Discussion

room-

Class room

Clinical Patho.Pharmacology

Facilitators

Clinical phato. &Pharmacology

8April 8th

2015Evaluation 09.00-11.00 09.00-11.00 Class room LECTURER,

FACILITATORS.



Clinical Neuroscience Semester IVTopic and Schedule Regular and English Class

Date Topic/Module Class B Class A Venues Conveyer1

April 9th

2015

Vertigo, bell’s palsy and Meniere DiseaseHearing loss and TinnitusIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class roomClass room

Disc. Room

Class room

dr. IA Sri Wijayanti, M.Biomed, Sp.Sdr. Made Wiranadha Sp.THTKLFacilitators.

Topik: Cerebral PalsyLesi batang otakdr. IA Sri Wijayanti, M.Biomed, Sp.Sdr. Made Wiranadha Sp.THTKL

2April 10th

2015

Kejang Demam (pediatric)Seizure, Epilepsy and Status EpilepticusIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Dewi Sutriani Maharini, Sp.A

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

Facilitators.

Topik: Duchene muscular dystrophy, pina Bifida, fenilketonuriadr. Dewi Sutriani Maharini, Sp.A/Dr.dr. DPG Purwa Samatra, Sp.S(K).

3April 13th

2015

Tension Headache and ClusterImaging interpretasi x-Ray tengkorak dan tulang belakangIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Class room

Disc. Room

Class room

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

Facilitators.

Topik: artritis kranial, CT can otak dan interpretasidr. Made Oka Adnyana, Sp.S(K)/dr. Made Widhiasih, SpRad

4April14th

2015

Migren and Neuralgia TrigeminalImagingIL/Self Ass.SGDBreak.

08.00-08.30

08.30-09.0009.00-10.3010.30-12.0012.00-12.30

09.00-09.30

09.30-10.0010.00-11.3013.30-15.0011.30-12.00

Class room

Class room

Disc. Room

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

Facilitators.



Student projectPlenary

12.30-14.0014.00-15.00

10.00-11.3015.00-16.00 Class room dr. Made Oka Adnyana,

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

5April15th

2015

HNP, Radicular syndrome, Neurogenic BladderAcute and refered painIL/Self Ass.SGDBreak.Student projectPlenary

08.00-08.30

08.30-09.0009.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-09.30

09.30-10.0010.00-11.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Kumara Tini, Sp.S, FINS

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

dr. Kumara Tini, Sp.S, FINS/ Dr. dr. Pt. Pramana, Sp.AN.,M.Kes.

6April16th

2015

Dementia/Alzheimer

Movement Disorder/NeurogeriatricIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Eka Widyadharma, M.Sc,Sp.S(K)dr. IA Sri Wijayanti, M.Biomed, Sp.S

Facilitators.

Topik: Alzheimer, MCI, Afasia, gangguan gerak lainnyadr. Eka Widyadharma, M.Sc,Sp.S(K)/dr. IA Sri Wijayanti, M.Biomed, Sp.S

7April17th

2015

CTS, TTS, peroneal palsyNeuropathic pain, neuropati, HNPIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Class room

Disc. Room

Class room

dr. Eka Widyadharma, M.Sc,Sp.S(K)dr. Eka Widyadharma, M.Sc,Sp.S(K)Facilitators.

Topik: ALS, Multiple sclerosis

dr Eka Widyadharma, M.Sc,Sp.S(K

8April 20th

2015

CNS Tumor primer dan sekunderTraumatic Brain Injury, hematom epidural, hematom subdural.IL/Self Ass.SGDBreak.Student projectPlenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.0014.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.3015.00-16.00

Class room

Class room

Disc. room

Class room

dr. Made Susilawathi, Sp.S

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

Facilitators.

Topik: hidrosefalusdr. Made Susilawathi, Sp.S/ Prof. Dr. dr. Sri Maliawan, SpBS(K)

9April 21st

2015

TIA, Infark cerebral, hematoma intraserebral, SAHStroke 2 ( manage )

08.00-09.00

10.00-10.30

09.00-10.00

11.00-11.30

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



Stroke 3 ( surgical )

IL/Self Ass.SGDBreak.Student projectPlenary

10.30-11.00

09.00-10.0011.00-12.3012.30-13.0013.00-14.0014.00-15.00

11.30-12.00

10.00-11.0013.30-15.0013.00-13.3012.00-13.0015.00-16.00

Disc. room

Class room

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

Facilitators.

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

10April 22nd

2015

Trauma Medula spinalis, Complete spinal transection, acute medulla compressionAmnesia Pasca TraumaIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.0009.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.0010.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Disc. room

Class room

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

dr. IGN. Budiarsa, Sp.S

Facilitators.

Topik: sindrom kauda equina, Siringomyelia, mielopati, dorsal root syndromeDr.dr. TjokordaGB. Mahadewa, M.Kes., SpBS(K)Spinal/dr. IGN. Budiarsa, Sp.S

11April23th

2015

GBS, Myastenia GrafisEnsefalopati, KomaIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.3008.30-09.0009.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.3009.30-10.0010.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Disc room

Class room

dr. IGN Budiarsa, Sp.Sdr. Kumara Tini, Sp.S, FINS

Facilitators.Topik: Mati batang otak, syndrome hornerdr. IGN Budiarsa, Sp.S/dr. Kumara Tini, Sp.S, FINS

12April 24th

2015

Meningitis, ensefalitis, malaria serebral, RabiesCNS HIV/AIDS, Poliomielitis, tetanus, tetanus neonatorumIL/Self Ass.SGDBreak.Student project

Plenary

08.00-08.30

08.30-09.00

09.00-10.3010.30-12.0012.00-12.3012.30-14.00

14.00-15.00

09.00-09.30

09.30-10.00

10.00-11.3013.30-15.0011.30-12.0010.00-11.30

15.00-16.00

Class room

Disc room

Class room

dr. Susilawathi, Sp.S

dr. Indrasari Utami, Sp.S

Facilitators.

Topik: infeksi sitomegalo virus, toksoplasmosis serebral, abses otakdr. Susilawathi, Sp.S/dr. Indrasari Utami, Sp.S

April 27th

2015

April 28th

2015

April 29th

2015

Basic clinical skillFungsi saraf kranial

Basic clinical skillMotorik, koordinasi, sensorik

Basic clinical skillFungsi luhur dan refleks

08.00-11.00

08.00-11.00

08.00-11.00

11.00-13.00

11.00-13.00

11.00-13.00

Skill Lab

Skill Lab

Skill Lab

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

dr. I Putu Eka Widyadharma, M.Sc, Sp.S(K)

dr.DSK. Indrasari Utami, Sp.S



April307th

2015

May 4th

2015

Basic clinical skillTulang belakang dan meningeal sign, tanda ischialgia

Basic clinical skillPemeriksaan DiagnostikRadiologi dan elektrodiagnostik

08.00-11.00

08.00-11.00

11.00-13.00

11.00-13.00

Skill Lab

Skill Lab

dr. Ni Made Susilawathi, Sp.S

dr. Kumara Tini, Sp.S, FINS

May 7th

2015 EVALUATION 08.30-10.30 08.30-10.30

Team lectures :1. dr. Wayan Suarya, PAK.2. dr. I Ketut Karna, AIF., M.Kes.3. Prof. Dr.dr. Nyoman Mangku Karmaya,

M.Repro.4. dr. I Wayan sugiritama, M.Kes.5. Dr. dr. I Made Jawi, M.Kes.6. dr. Ida Bagus Ngurah, M.For.7. dr. A.A.B.N. Nuartha, Sp.S(K)8. Dr. dr. DPG. Purwa Samatra, Sp.S(K)9. dr. I Made Oka Adnyana, Sp.S(K)10.dr. IGN. Budiarsa, Sp.S11.dr. Desak Ketut Indrasari Utami, Sp.S12.dr. I Putu Eka Widyadharma, M.Sc.,

Sp.S(K)13.dr. Kumara Tini, Sp.S, FINS

14.dr. I.A Sri Wijayanti, M.Biomed, Sp.S15.dr. Made Susilawathy, Sp.S16.dr. Dewi Sutriani Maharini, Sp.A17.Prof. Dr. dr. Sri Maliawan, Sp.BS(K)18.Dr.dr. Tjokorda GB. Mahadewa, M.Kes.,

Sp.BS(K)Spinal19.dr. Wayan Niryana, M.Kes, Sp.BS(K)20.dr. Made Wiranadha Sp.THTKL21.Dr.dr. Putu Premana Suarjaya, Sp.An.,

M.Kes.22.dr. Made Widhi Asih, Sp.Rad23.dr. Ni Putu Sriwidyani, Sp.PA24.dr. I Nyoman Wande, Sp.PK



LEARNING PROGRAME BASIC NEUROSCIENCE

Day 1st

NEUROPHYSIOLOGYdr. K. Karna, PFK, M.Erg.

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

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

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

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

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

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

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

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

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

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

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



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

a. The neuron is the basic structural and functional unit of the NS, which typically consist of a cell body (soma), several dendrites, and a single axon. Neuron structure is related to function, which have receptive and integrative zone (dendrite and cell body), trigger zone (axon hillock), and conductive region (axon) especially in terminal end of axon has secretive synaptic transmitter.Electrochemical activity in neuron include- Membrane potential: polarization, depolarization, repolarization, hyperpolarization.- Graded electrogenesis: i.e graded potential, receptor potential, EPSP, IPSP.- Site of origin of conducted impuls (action potential), all or none transmission, incoming

signal in terminal end of the axon as trigger to secreting transmitter synapticNeuron communicate with muscle, gland, and other neurons at junction its called neuromyal junction, neuroglandular, and synapses. Synapses are found in dendrite, soma, and axon (axodendrtic, axosomatic, axoaxonic synapses).

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

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

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

II. SELF – STUDY , ESSAY QUESTION

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

during the production of an action potential.7. Explain how action potentials are regenerated a long myelinated and non myelinated axon..8. Describe the events that occur in the interval between the electrical excitation of axon and the

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

categories and explain how tonic and phasic receptors differ 12. Describe the classification of the sensory division – sensory receptors.13. Give examples of different types of cutaneous receptors (somatosensory receptors) and describe

the neural pathways for the cutaneous senses



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

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

16. Distinguish between and compare monosynaptic and polysynaptic reflexes.

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

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

the nerves to his arm2. What is a thorough general physical examination should be made in this case.3. Which one of the sensory test should be done4. Which one of the reflex test should be done5. Describe general physical examination should always be done in motor system of this 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 sclerosis1. Why the conduction of nerve impulses may be slowed or blocked.

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

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

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

Day 2nd

NEUROPHYSIOLOGY dr. K. Karna, PFK, M.Erg.

I. ABSTRACT1. The motor division of the NS as responsible for controlling a variety of bodily activities such

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



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

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

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

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

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

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

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

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

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

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

Day 3rd

NEUROANATOMYdr. I Wayan Suarya, PAK.

AIMS: 1. Describe the common function, special characteristic, structure and division of nervous system,

spinal cord.2. Describe the features, parts, structure function of brainstem, localization of the ascending and

descending tracts in the brainstem,.3. Describe of cranial nerves, functional structures (general and special), and clinical examination of

cranial nerves lesion.

LEARNING OUTCOME:Describe the common function, special characteristic, anatomical structure and division of nervous system, spinal cord.

1. Describe structure and division of neuron, neuroglia, synapse.2. Describe the parts, white and gray matters nuclei, tracts of the spinal cord.3. Describe source, purposes and journey of each tracts.4. Describe upper motor neuron (UMN), lower motor neuron (LMN), and clinical

differentiations of lesion of UMN versus LMN.5. Describe 12 couples of cranial nerves: nuclei, receptors, effectors and qualities of each cranial

nerves.6. Describe the formations of brachial and lumbo-sacral plexuses.7. Describe topography of the cranial nerves nuclei in the brainstem.



CURRICULLUM CONTENTS:1. General function, special characteristic, anatomical structure and division of nervous system,.2. Division of neuron, neuroglia and synapses.3. Parts, structure in white and gray matters of spinal cord.4. Sources, purposes and how the journey of each tracts.5. Parts of nuclei of the gray matter of spinal cord.6. UMN, LMN, the structures or parts, how the journey and clinical differentiations

lesion of UMN versus LMN.

ABSTRACTS OF LECTURES:Nervous system have 2 parts: that are Central nervous system (CNS) and pheripheral nervous

system (PNS) and have base characteristics: that are irritability and conductivity so that human being may to integrate with internal and external enmvironments. Main component of nervous system are: neuron, neuroglias and blood vessels. Base anatomical structure of nervous system is neuron, base physiological structure is reflex arc. The neuron divide by measure (4-120 micron): small, moderate and great; and by cytoplasmic protrusion: unipolar, bipolar and multipolar (type I and II). One neuron to the others be contact/connect as: synapse (synapsis). In synapse be related with a substance: neurotransmitter. The reflex arc in simple reflex is receptor, afferen/sensory, efferen/motor, effector; intercalate neuron or interneuron addition in the complex or coplicated reflex. Reflex is very impoprtant and routine examination in neurological clinic. Many stimuli have receptor alone. Neuroglias divide to 3 parts: astrocyte, oligodendroglia and microglia. The CNS have special characteristic on base vascularisation.

Spinal cord is part of CNS located in vertebral canal have cervical, thoracal, lumbal, sacral and coccygeal parts. Superficial part is white matter consist nerve fibers: tracts (ascending, descending and intersegmental tracts), deep/profundus part cosist cell bodies of neuron: nucleus/nuclei. The tract have origin/source, route/journey, function and purpose alone. From spinal cord come out average 31 couple spinal/segmental/or intervertebral nerves, its have supply qualities: general somatic sensory and motor, symphathetic fibers (Th. 1-L2/3) and parasymphathetic fibers (S 2 3 4) at addition.. Innervation to skin knows by skin segmental innervation or dermatome innervation. Spinal cord receive blood from ventral and dorsal spinal arteries branches of vertebral arteries, and radicular arteries branches of intercostal/ subcostal arteries.

Brainstem (truncus encephalicus) have 3 parts: medulla/medulla oblongata, pons, midbrain/mesencephalon is very important because have center of cardiovascular, respiratory system and primary conciousness. The brainstem also pass through by ascending, descending tracts and filled in most of the nuclei of cranial nerves. Cranial nerves may contribute by the qualities: general somatic efferent, general visceral efferent, general visceral afferent, general somatic afferent, special somatic (branchial) efferent (special visceral/branchial efferent-in American and England library), special somatioc afferent, special visceral afferent. Motor nuclei of cranial nerves innervate by UMN (upper motor neuron-corticonuclear/corticobulbar fibers) divide manner: bilateral, homolateral or contralateral and with or without intercalate neuron. UMN (upper motor neuron-corticospinal/pyramidal tract) also innervate nuclei in ventral corn of spinal cord. LMN (lower motor neuron): origin in ventral corn of spinal cord and motor nuclei of cranial nerves. Clinical sign and sympthom lesion of UMN compare with LMN are different, and very important and routine examine in neurology clinic. Lesion on some cranial nerves are routine examine in neurology clinic, by examination the receptors or effectors each innervations.

Each cranial nerves have nucleus in brainstem except the olfactory, optic and accessory nerves. Their nuclei have certain position (tophography). The cranial nerves have their own receptors, effectors



and destination. It is very important in clinical aspects. Cranial nerves may have only one, two or more qualities. UMN innervate motor nuclei by homolateral, bilateral or contralateral manner, with or without intercalate neuron.LMN innervate the effector by homolateral or contralateral manner.Generally the spinal nerves have two kinds of qualities: general somatic afferent andefferent, but from the thoracal 1 to Lumbal 2 or 3 there are addition of [presynaptic symphathetic fibres which go directly to paravertebral or prevertebral ganglia except the fibers which go to adrenal medulla. In sacral segment (S 2 3 4) There are presynaptic/prganglionic fibres that going intrinsic parasympathetic ganglia supplying mainly genitalia organs. The parasympathetic centers are also found incranial nerves nuclei that why it is called craniosacral nerve, and the sympathetic nerve is called thoracolumbal nerve. In cervical 5 6 7 8 thoracal 1 the spinal cord compose of widening segment it called intimescentia, as the origin of motor neuron for anterior rami to form brachial plexus ( 5 rami 3 trunks 6 devisions 3 fasciculus/cords) 5 main nerves for the upper limbs. Lumbosacral plexus (divide to lumbar and sacral plexuses) formed by ventral rami of (L1) L2 to S 4 innervate lower limbs, internal organs in pelvis including genital organs.

TRIGGER/SCENARIO:Case 1:A man 35 years old who had a stab trauma on spinal cord. After CT scan he had hemisectio/half lesion left spinal cord on thoracal 10. He had hospitalization in neurology department. Two week after to hospital a neurologist take examination the patient: a. power, b. trophy, c. tone of muscles, d. stretch, pathological and superficial reflex, e. clonus. e.sensibility.

LEARNING TASK:1. Describe the power of muscles on: left and right upper limbs and lower limbs?2. Describe the muscle tone of: left and right biceps brachii, left and right quadriceps femoris, left and

right triceps surae?3. Describe the the trophy of each muscles above?4. Describe the pain and temperature sensation on: left and right upper limbs, left and right lower

limbs, left and right the body?5. Describe special sensation on left and right upper limbs, left and right lower limbs, left and right the

body.6. Describe the Babinski reflex? Where that reflex examine by doctor? Why the manner /method.7. Describe the route, purpose, main purpose, last purpose of lateral spinothalamic and gracile,

cuneate tracts.8. Describe the route, parts, purpose of pyramidal tract (cortico spinal, corticobulbar tracts), and how

the innervation manner to the motor nuclear of cranial nerves.9. Please list the other tracts: routes and purposes (homo, contra or bilateral).

Case 2:Child, male 10 years old had fever 7 days. After go and examine in hospital has found the child suffering poliomyelitis. Left lower limb can not movement.

LEARNING TASK:1. Describe main deficit the movement on left lower limb?2. Describe the part of nuclei of spinal cord attack?3. Describe the sensibilities senses on left lower limb?4. Describe the reflex, tone and trophy of left lower limb?



5. Describe the Babinski reflex on left lower limb?What are you know about Babinski reflex?

Case 3:A man 65 years old, 80 kgs body weight, 160 cm of height. He very busy, can not exercise, a smoker average15 of cigaretes a day from 20 years ago. He have hypertension: T: 190/90 mm Hg. Three days ago he can not movement left lower limb, and his right eye adduct.

LEARNING TASK:1. Describe the lower limb can not movement? What tract affected, and where the location lesion

affected.2. Describe the route of corticospinal tract, and route of tract and nerve that innervate lateral rectus

muscle of eye?3. Describe the others cranial nerves nucli innervate by corticonuclear tract?4. Describe the other muscles of orbita innervate by Cranial nerves III, IV and VI?5. Describe The others cranial nerves nuclei innervate by cortico-nuclear tracts.6. Describe the foramen/fissure as the ways of cranial nerves.7. Describe the formation of brachial plexus, and at last 5 main peripheral nerves innervate upper

limbs? Please make a diagram of plexus brachialis!8. Describe the lumbosacral plexus, and mention 4 main peripheral nerves from lumbosacral

plexuses!9. Describe are the qualities of peripheral nerves from lumbosacral plexuses!

Case 4:A craftsman of metals 45 year old, until one month his hand lost of heat sensation.Neurologist examine him with CT scan. He affected the syringomyelia on cervical 5678 thoracal 1.

LEARNING TASK:1. Describe the tract affected?2. Describe the part of spinal cord route of the tract above?3. Describe the formation of the brachial plexus? Please make the diagram.4. Describe the qualities of plexus to innervate the upper limbs?5. Describe the differences lesion of: rami anterior and posterior, lesion in dorsal radices, anterior

radices, all of dorsal division, one of fascicle/cord?

Day 4th

NEUROANATOMYdr. I Wayan Suarya, PAK.

AIMS: Describe the structure FR (formatio reticularis), cerebellum and telencephalon.

LEARNING OUTCOME:1. Describe the parts, structures of cerebellum.2. Describe the connection of brainstem and cerebellum.3. Describe of the intrinsic structure, cytoarchitectonic of cortex cerebellum.4. Describe the tracts to and out of cerebellum, and each route.



5. Describe the clinical aspect the lesion of the cerebellum.6. Describe part, sulcus, fissure, gyri of the cerebrum.7. Describe architectonic structure, and interconnection of neuron in isocortex (cerebral cortex), and

functional areas of cerebral cortex.

CURRICULUM CONTENTS:1. Components, borders, and surface features of the brainstem.2. Topography cranial nerves nuclei in brainstem.3. Come out of the cranial nerves from ventral aspect of the brainstem.4. The structure of fourth ventricle.5. Functional structure and clinical aspect of cranial nerves6. The parts, intrinsic structure, cytoarchitectonic of cortex cerebellum.7. The connection cerebellum with: brain, brainstem, spinal cord.8. Structure of pedunculi, corpus medullare of cerebellum.9. Functional Clinical aspect of cerebellum.10. Cerebrum or hemispherium cerebri: parts, sulcus, gyrus.11. Architectonic structure, interconnection of neuron in cerebral cortex and its funtional areas.

ABSTRACT OF LECTURE:FR (formation reticularis) in neruoanatomi is the term that include brainstem substance filled in the space between specific nuclei and tracts in the brainstem. FR sophisticated structure that consist many kind of neurons.Obey Cajal, the neurons in FR consist orde III of sensory fibers. Obey Brodal (1957) that are consist specific area and have cytoarchitectonic and have specific intrinsic organization.Intrinsic Organization:

1. In medulla (medulla oblongata) have 5 nuclei, and have each connection (afferent and efferent) of each nucle.

2. In Pons (FR Pontis): have 3 parts of nuclei.3. In midbrain (FR mesencephali): have 3 nuclei. Sukardi, E., Chapter 15.

The neurotransmitter and FR:Monoamine fibers build by the axons that have monoamine: nore-adrenaline, serotonin and dopamine. The research indicate most of its source from special area of the FR. The broad lined mono-amine fibers consist 5: noradrenergic descending, noradrenergic ascending, noradrenergic from locus ceruleus, serotonergic ascending and dopaminergic fibers. Except dopaminergic fiber, the fibers from the FR of brainstem. Please look at the table on Sukardi, E., page: 191-192.Many functional aspect of FR: - facilitation area, inhibition area, respiratory center, cardiovascular center, Primary consciousness center, On these had many research: Torvik and Brodal (1957, Brodal and Rossi (1955) Kuypers (1958). The corticonuclear fibers consist 2 parts: 1), direct and 2) indirect fibers.

The Cerebellum is suprasegmental part of CNS, located dorsal of brainstem filled in posterior of cranial cavity and connect with brainstem by three couples of structure called: pedunculi cerebelli (superior/anterior/brachium conjunctivum, medius/brachium pontis, posterior/inferior/corpus restiforme), its function is pass by afferent and efferent fibers. Cerebellum divide to 3 parts: archeocerebellum, paleocerebellum, and neocerebellum. Archeocerebellum is the oldest part had functional connection with vestibular nuclei, paleocerebellum receive impulses from spinal cord through the spinocerebellar tracts (ventral and dorsal) and cuneocerebellar tract (fibrae arcuatae externae), conduct proprioceptive impulses. In medial part have vermis and lateral part have hemispherium.



Intrinsic structure of cerebellum: cortex, medullary and nuclei parts. In cortex there are fissure, folium; in medullary part there is white matter filled by nerve fibers arbor vitae. Cerebeller nuclei (nuclei cerebella) there are 4 couples, from medial to lateral: Fastigii, globusus, emboliformis, and dentatus, its located dorsal and dorsolateral of fourth ventricle of brain (ventricle IV / ventriculus quartus). The cortex of cerebellum have 3 layers: molecular, piriform, granular layers/stratum.Afferent fibers divide divide to 2 parts: Climbing and mossy fibers. All of impulses to the cerebellum are excitation to neuron of cortex and nuclei of cerebellum. But, Purkinje cells inhibition, connection with the nuclei of cerebellum, lateral vestibular nucleus, basket cells and all of the interneurons in cerebellar cortex.Efferent impulses can reach to red nucleus, thalamus area 4 Brodmann by thalamo-cortical fibers. By these tracts (Rubro-spinalis, rubroreticularis-reticulospinalis tracts) cerebellum can coordinate the motoric reaction ( in a reflex, automatic and aware manner). Muscle tone controlled by cerebellum through reticulospinal tract (alpha and gamma motoric neurons). White matter of cerebellum divide to 2 parts: intrinsic (cortico-nuclear, association fibers) and extrinsic fibers( in the corpus restiforme, brachium pontis and brachium conjunctivum). In caudal cerebellar peduncle had 8 tracts, medial cerebellar peduncle had 1, in cranial cerebellar [peduncle had 2 tracts/fibers.Functional aspect of cerebellum: 1. Controlled the tension of muscles in equilibrium and posture; 2. Guarantee on fast and regulated contraction group of muscles.Neocerebellum lesion mainly have sympthom, smooth action disorders: 1. Hippotoni and asthenia, 2. Asinergi, 3. Nystagmus.

Telencephalon have 2 parts: telencephalon impar, and a couple cerebral hemisphere. Cerebral hemisphere left and right connect with caloosal body (corpus callosum). Cerebral surfaces showed out : sulcus or fissurae and gyrus; most of cerebral cortex hidden in sulcus or fissurae. One hemisphere have 4 lobe, and each lobe have gyrus. Cerebral cortex divided to 3 parts: neocortex/ neopallium/ isocortex, paleocortex/ paleopallium, archicortex/archipallium. Koniocortex applied to sensory part of cortex: optic area, auditory area and somesthetic area. Isocortex had 6 layers, had many connections of each neurons in each layers. Lorente de No (1949) had studied main connections neuron to neuron in the isocortex. Brodmann (1909) had studied functional area in cerebral cortex. Most of the cerebral cortex had studied, numberized and had studied each fuction. That are primary, assosiation, integrated, ideomotor area in cerebral cortex.

Structure of white matter of cerebral hemisphere; this substance filled in between cerebral cortex and subcortical substance. Fibers of the white matter cerebral hemisphere divide ti 3 main parts: Projection (afferent and efferent), assossiation and commissural fibers. Projection fibers divided 2 parts: source from cerebral cortex and from subcortical center.From corona radiatacapsula interna/ internal capsule (crus anterior, genu, crus posterior). Each parts of capsula interna filled in (arranged) by each tract alone.Commissural fibers mainly connection same center to the other hemisphere, but assosiation fibers connection the other cortex in same hemisphere. Commissural fibers divide to 3 parts, association fibers to 4 parts.

Case 1: A man 65 years old had a progressive headache since 3 month ago. He have examination in hospital: the intracranial tension increase, tremor, ; The CT Scan: Tumor on the cerebellum.

LEARNING TASK:



1. Describe the FR (Formatio Reticularis) in medulla, pons, and midbrain.2. Describe the connections (afferent and efferent) of each fibers.3. Describe the neurotransmitters in FR, and make the diagram sources and transmissions of each

fibers.4. Describe of many functionaspecty of FR, locus ceruleus.5. Describe the positions of: LM (lemniscus medialis), Lemniscus trigeminalis, Tractus

spinothalamicus lateralis, fibrae corticonuclearis, fasciculus pyramidalis, rubrospinalis, vestibulospinalis, tectospinalis, and assossiation fibers in midbrain.

6. Describe the prediction of neurologic manifestation result the lesion on paramedian or lateral of midbrain.

7. Describe the position and connection of cerebellum to the brainstem.8. Describe the afferent, efferent connections and functions of archi-, paleo-, neo-cerebellum.9. Describe the projection from cortex of cerebellum to the nuclei.10. Describe the projection of olivary nuclei to cortex of cerebellum.11. Describe the excitation, inhibition fibers in cerebellum.12. Describe the kinds of circuit in cortex of cerebellum.13. Describe the pedunculi of cerebellum and the fibers throw in.14. Describe some disorders in cerebellum: nystagmus, hippotoni, asteni, asinergi.15. Describe the sulci, gyri, on brain: from medial and lateral aspect.16. Describe the areas of brain, and each function of its.17. Describe the allocortex, sensory and motor homunculus.18. Describe the term: alexia, agraphia, apraxia, and limbic system.19. Describe the location and representation of learning, memory functions.20. Describe the projection, commissural and association fibers of the brain.

DAY 5th

NEUROANATOMYdr. Wayan Suarya, PAK.

AIMS:1. Describe the structure of: telencephalon, cerebral cortex, white matter of cerebral hemispheres

and diencephalon., its connection with the other parts of CNS, and ganglia basalia.2. Structure and route of visual and olfactoric system, intracranial meninges ventricle of CNS,

vascularisation, general development, evolution of CNS.

LEARNING OUTCOME:.1. Describe the limbic system, emotion and high function of CNS.2. Describe composition of white matter of cerebral hemispherium: projection fibers, internal capsule,

commissural fibers, and assossiation fibers.3. Describe structure, each connections and clinical aspect of ganglia basalia.4. Describe differentiation of pyramidal and extrapyramidal system.5. Describe structure of of olfactory nerve, rhinencephalon.6. Describe composition of intracranial meninges, ventricle system of brain.7. Describe general and regional vascularisation, arterial circle, and venous system of the brain.

CURRICULUM CONTENT:1. Limbic system and other structure in emotional reactions, memory and learning.2. Composition/structures of white matter of the cerebral hemispherium: projection fibers, internal

capsule, commissural fibers, and assossiation fibers.



3. The structure/component of the ganglia basalia, the connections and clinical aspect of ganglia basalia disorders.

4. Differentiations of pyramidal and extrapyramidal systems.5. Structure of olfactory nerve and the other parts of brain involve in smell process.6. Composition of intracranial meninges, duramateric sinus system and ventricular system in the

brain.7. General and regional vascularisation of brain, arterial circle, and venous system of the brain.

Abstracts of lectures:Diencephalon and ganglia basalia constitute subcortical nuclei (gray matter) of the cerebral

hemisphere together. Diencephalon divided to: Thalamus, metathalamus,hypothalamus, subthalamus, epithalamus. Thalamus oval shape of gray matter, have average long: 3 cm, lateral to ventricle III. Thalamus have many group of nucleus, but functionally divided to 3 parts:Specific/ relay connection, association nuclei and subcortical projection nuclei. Functional and clinical aspect of thalamus: except olfactory impulse, all of the impulses send to the nuclei of thalamus. Olfactory fibers have not synapse in thalamus, but projection directly to the rhinencephalon. Structure and orgization of thalamus just not only relay station of the sensory impulses send to the cerebral cortex, but so far complex. Many function commonly connected to thalamus: main sensory integration, part of thalamus regulate conciousness and alertness, connect in emotion aspect, integrated center of motoric function ( because it receive main efferent projection from cerebellum and striatum body/corpus striatum).

Hypothalamus and hypophysis cerebri: hypothalamus most ventrally parts of diencephalon. In man slightly over than 4 gram, take place very important nerve mechanisms. So that hypothalamus divided to 3 parts: supraoptic, tuberal, mammillary parts. Hypothalamus have wide and complicated connection to the other nervous center. Hypothalamus have afferent, efferent connections. Main functions of hypothalamus to a).endocrine and b).to ANS in brainstem and spinal cord (autonomic descendens fibers), and c). Center of expression of emotion,d) correlation the visceral and olfactory impulses.Hypothalamus connect to brainstem by: 1). Periventricular fibres, 2). Hypothalamoreticular fibers, 3). Mammillotegmental fascicles/fibers.

Rhinencephalon only included CNS structure its receive nerve fibres from olfacfory bulbs. Another meaning rhinencephalon included: olfactory bulbs, olfactory tracts, olfactory striae, anterior perforate substance, part of amygdaloide body, and part of prepiriform cortex, ( it is appropriate to paleopallium). The conduction machanism of olfactory impulse: olfactory cells in nasal mucosafila olfactoria (foramina in cribriform/crbrose lamine at ethmoidal bone dendrite of mitral cells in olfactory bulbs (its take place upper than roof nasal cavity).Amount of olfactory cells there are synaptic connection with one mitral cell. These synaptic knows glomerulus. Axons of mitral cells formed olfactory tracts, and there are have collateral fibres and formed synaptic connections with granular cells in olfactory bulbs, and axon of granular cells formed synaptic connections dendrite of same mitral cells form feedback arc (circuit). To posterior part the olfactory tracts have three branches;stria olfactoria (lateralis, medialis and intermedia). These cortex are the primary center of olfactory, the function is olfactory perseption. Area 28 and 33 there are a higher center of olfactory, functionally for olfactoric gnosia, identification of smell.

Intracranial meninges, like in spinal cord, duramater, arachnoid and piamater. Arachnoid and piamater layers knows leptomeninx, and duramater knows pachymeninx. Duramater divided to 2 layers: outer layer rich with blood vessels and nerves and lining inner surface of cranial bone and constitute periost layer, and inner layer, thinner, and linning with a layer of thin cells. Generally two these layers adhering to the other except in certain places: duramater sinuses (sinus duramateris). These sinuses filled in venous blood ( from superficials cerebral veins.



Duramater also formed: falx cerebri, tentorium cerebelli, falx cerebelli, and diaphragma sellae. Subarachnoidal cavity: cerebellomedullar cistern, pontis cistern, interpeduncular (basal) cistern take place on the brainsten. The composition of duramater sinuses there are formed by: Superior and inferior sagittal sinuses, rectus sinus, confluens sinuum, transverse sinus, sigmoidal sinus, covernous sinus. Transverse sinus internal jugular veins, anterior direction cavernous sinuses connect with angularand facials veinsophthalmic veins, so that duramater sinuses had connection with extracranial veins. Posterior direction cavernous sinussigmoid sinus by (through) superior and inferior petrosus sinuses. Two main function of CSF are: (1) as venous system in brain, (2) location of absorption of Th CSF through arachnoidal villimainly to superior sagittal sinus.Cerebral ventricles there are: lateral, tertius (III), mesencephalic aquaduct, quartus (IV) and central canal.

Brain vascularisation there are depend on aerobicglucose metabolism. In brain cells or tissue be found a small amount of glucose and oxygen. Brain is 2 % of body wight, purpose 17 % of cardiac output, may be 20 % of gas oxygen of body purposes.Many main factors the circulation of the brain are: blood gases, brain metabolism, otoregulation. Many pathological disorders are result of circulation of the brain. The brain receive blood from two couple of ateries: internal carotis and vertebral arteries. Internal carotis artery beside participate in arterial circle it give branches: ophthamic, posterior communicans, anterior choroid, anterior cerebral and medial cerebral arteries. Vertebral arteies beside serve to spinal cord, brainsten and cerebellum, it follow give its terminal branches to form arterial circle (circulus arteriosus): posterior cerebral arteries.Regional vascularisation: the parts of the brain there are had each arteries and its branches. The venous blood circulation of the brain: veins of the brain had qualities: (1) Not follow the artery, (2) had thin of the wall, (3) deep veins of the brain not have a wide anastomosis, (4) most of superficial cerebral veins pour blood to superior sagittal sinus, and many pour to tranverse sinus, in the contrary direction to blood flow in duramater sinus relevant. Venous system in the brain divide to 2 group: superficial and deep veins.

Case 1: A man 50 years old affected Diabetes mellitus until 10 years ago. The diabete is not controll carefully. Three days ago he had strok affected on branches of vertebral artery: left posterior inferior cerebellar artery and left posterior cerebral artery. The arteries lesion to knows by CT scan.

LEARNING TASK:1. Describe the corona radiate in internal capsule, afferent and efferent projection fibers.2. Describe the position of the fibers in the internal capsule, and to predict the neurological symptoms

and signs of one side internal capsule lesion.3. Describe the thalamus with the others components of diencephalon.4. Describe the position of thalamus concerning third ventricle.5. Describe the connections of the thalamic nuclei.6. Describe the main function of thalamus.7. Describe the signs on the upper case.8. Describe the nuclei of hypothalamus, and each functions of its.9. Describe the connection of each parts of ganglia basalia.10. Describe the control mechanism of hypothalamus to pituitary gland, brainstem, ANS (autonomic

nerve system), hunger and thirsty center.11. Describe the connection of ganglia basalia to control the skeletal muscle movements.

Case 2:



A Man 50 years old affected Diabetes mellitus until 10 years ago. He is not control be carefully. Three days ago he had stroke, affected on branches of vertebral artery: left anterior cerebellar artery (by CT-Scan).

LEARNING TASK:1. Describe the left posterior inferior cerebellar artery, left cerebral artery joins to forming arterial circle

(circulus arteriosus), and the athers arteries forming it.2. Describe the lobe, area on the brain serve by: posterior, medial, anterior cerebral arteries.3. Describe the area Broca, precentral, poscentral, internal capsule, thalamus, hypothalamus,

pituitary gland, serve by………..arteries.4. Describe the differencies venous system on brain compare with the common venous system in the

body.5. Describe the intracranial meninges to built the sinus duramateris, and where the liquor

cerebrospinalis to produce.6. Describe the oxygen comsumption of the brain.

Case 3:A Physician work in forensic department, after autopsy he had bad smell until 2-3 days, where as he have taken a bath and wash cloth and his hair.

LEARNING TASK:1. Describe the physician have bad smell until 2-3 days after autopsy.2. Describe the components to forming the circle the nerve of bad smell.3. Describe the parts of brain involve in olfactory system, and the receptor.4. Describe the receptor, route, stria of the olfactory system.

Case 4:A neonatal baby have congenital anomaly on his back; and he had diagnosed by the physician: Spina bifida. On the skin of head the child had pyodermia. Also diagnosed: had meningitis, spread from piodermia.

LEARNING TASK:1. Describe the piodermia may spread to the intracranial meninx.2. Describe the components of meninges, and sinus duramateris.3. Describe the CSF: produce, flow from plexus choroideus right atrium of the heart.4. Describe the subarachnoidal space filled in.5. Describe general development of brain.6. Describe some development disorders, and the level of main organization in nervous system.

DAY 6th HISTOLOGYHISTOLOGICAL STRUCTURE OF NERVOUS SYSTEMdr. 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.

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.

LEARNING 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

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.

LEARNING 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!

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

LEARNING TASKS:

1. Brain tissue is protected from harmful microorganisms and hazardous materials by the Blood-Brain Barrier, please explain the components of Blood-Brain Barrier and describe its microscopic structure

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

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

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

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

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

NEUROPATHOLOGYdr. Ni Putu Sriwidyani, Sp.PA

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.

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

LEARNING TASK

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

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

LEARNING TASK

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

Case 3A 72 year old woman falls down the stairs. She does not lose consciousness. About 36 hours later, she develops a headache and confusion and is taken to the emergency department. On physical examination, she is conscious and has a scalp contusion on the occipital.

LEARNING TASKWhat is the most likely location of an intracranial hemorrhage in this patient?

SELF ASSESMENTDescribe and give some example of:

1. Cerebral edema, hydrocephalus, and raised intracranial pressure. 2. Malformation and developmental disease3. Trauma affecting CNS4. Cerebrovascular disease5. CNS Infection



6. Demyelinating disease7. Degenerative disease of CNS8. Tumors of CNS

DAY 7th Clinical Pathology dr. I Nyoman Wande, SpPKTOPIK : 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:1. 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?

PHARMACOLOGYDRUGS USED FOR SEIZURE DISORDERSDr. dr. I Made Jawi, M.Kes AIMS :

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

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

CURRICULUM CONTENT1. Basic pharmacology of anti seizure drugs

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

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

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

spread of electrical activity to adjacent neurons. There are several types and many causes of seizures. Identification of the cause of seizure activity is important in determining the type of therapy required. Contributing factors (e.g., head injury, fever, hypoglycemia, drug overdose) must be specifically treated to correct the underlying cause before chronic anticonvulsant therapy is started. Once the underlying cause is treated, it is rare that chronic antiepileptic therapy is needed. If the seizures are chronic and recurrent,



the patient is diagnosed as having epilepsy. Epilepsy is treated almost exclusively with anticonvulsant medications. The goals of therapy are to reduce the frequency of seizure activity and minimize the adverse effects of the medicine. To attain this, therapy must be individualized to consider the type of seizure activity and the age, gender, and concurrent medical condition of the patient. Patients as well as their families require education and support regarding their responbilities in managing epilepsy

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

LEARNING TASK1. Describe how you as a doctor would address this situation ?2. Describe anti seizure drugs using in seizure patients ?3. Describe adverse effect of anti seizure drugs using in seizure patients ?

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

PHARMACOLOGY MANAGEMENT OF PARKINSONISM & OTHER MOVEMENT DISORDERSDr. dr. I Made Jawi, M.Kes

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

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

CURRICULUM CONTENTDrug therapy for Parkinson’s Disease

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

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

producing cells in the portion of the brain responsible for maintenance of posture and muscle tone and the regulation of voluntary smooth muscles. Normally a balance exists between dopamine, an inhibitory



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

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

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

drug therapy to alleviate the 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 od

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

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

LEARNING PROGRAM CLINICAL NEUROSCIENCE

DAY 1st April 9th 2015.VERTIGO, MENIERE DISEASE AND BELL’S PALSYdr. IA Sri Wijayanti, M.Biomed, Sp.S

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

Learning outcome:

Can describe the:



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

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

AbstractsVertigo is an unpleasant disturbance of spatial orientation or illusory perception of movement of the body (spinning and wobbing) and/or of the surrounding that usually results in a disturbance of equilibrium system.The sense of balance (the equilibrium system) is provided by integration of inputs from the visual, proprioceptive, and vestibular system into the brain. Pathologies along these pathways results in dizziness with various forms and severity.Dizziness as general term, can be subdivided into vertigo, disequilibrium, and dizziness. 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 System2. Peripheral vestibular vertigo3. Central vestibular vertigo4. Non vestibular vertigo

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

well as the unpleasant sensation that room was spinning around him. The spinning resolved within 30 seconds but recurred again in the opposite direction when he rolled back to his original position. This had never happened to him before. The patient denied tinnitus, hearing loss, recent viral illness and head trauma.

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

(remember the secret seven and fundamental four)2. Make the physical examination of patient with imagination in correlation with the story above !3. How to differentiate between patient with peripheral and central vestibular vertigo?4. How to differentiate betweenvestibular 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 DISEASEAims:Describe diagnosis, initial management and/ or referral patients with meniere disease

Learning outcome:

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

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

AbstractsMeniere disease also called endolymphatic hydrops, is a disorder that can affect hearing and balance to a varying degree. Meniere disease is chronic disorder in inner ear, it’s not fatal but disturb the quality of life. It is characterized by episodes of vertigo, low-pitched tinnitus, and hearing loss. The hearing loss is fluctuating rather than permanent, meaning that it comes and goes, alternating between ears for some time, 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. Other conditions can present themselves with Meniere-like symptoms, such as syphilis, Cogan's syndrome, autoimmune inner ear disease, dysautonomia, perilymph fistula, multiple sclerosis, acoustic neuroma, and both hypo- and hyperthyroidism. 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. Sudden, severe attacks of dizziness or vertigo, known informally as "drop attacks," can cause someone who is standing to suddenly fall. Drop attacks are likely to occur later in the disease, but can occur at any time.

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

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

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

(remember the secret seven and fundamental four)2. Make the physical examination of patient with imagination in correlation with the story above !3. What is the differential diagnosis of this patient?4. Where is topical lesion on this case? 5. How to differentiate between Meniere and BPPV patient?6. Please explain the pathogenesis from each of differential diagnosis that has been mention above !7. What is the management of this patient ?8. When do we start to rehabilitate the patient ?

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

Learning outcome:

Can describe the:1. Diagnosis of Bell’s Palsy2. Differential Diagnosis of Bell’s Palsy3. Management for Bell’s Palsy4. Prognosis of Bell’s Palsy5. Further investigations and referrals

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

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

the exposure to cold preceded their symptoms. The face often described as feeling stiff and numb without any objective sensory deficit. Decrease tearing and hyperacusis may appear in some cases may precede weakness.



The condition is thought to be related to a viral infection, the swollen nerve being entrapment in the facial canal. Although not life threatening, Bell’sPalsy may have severe functional, aesthetic, and psychological consequences.

Self directing learningBasic knowledge that must be known:

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

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

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

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

(remember the secret seven and fundamental four)2. Make the physical examination of patient with imagination in correlation with the story above !3. What is the differential diagnosis of this patient?4. Where is lesion base on facial nerve pathway (make topical diagnosis)? 5. How to differentiate between facial palsy in Bell’s Palsy and Stroke patient?6. Please explain the pathogenesis from each of differential diagnosis that has been mention above !7. What is the management of this patient ?8. When do we start to rehabilitate the patient ?

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

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

HEARING LOSSdr. Made Wiranadha, Sp. THT-KL

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 Objective1. Describe general strategy in the approach to patients with hearing loss a trough history and

physical examination supported by selected and supporting tests or special technique investigations.

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

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

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

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

complication could be of the disease?

Case 2A 3 years old boy was brought to the ENT-HNS clinic with complaints has not been able to speak to the present, the patient does not respond when called upon. The patient does not respond well to hear the sound of thunder or a loud closed door.

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

FromMenner, A Pocket Guide to the Ear © 2003 Thieme

DAY 2nd April 10th 2015FEBRILE SEIZURE IN CHILDRENdr. Dewi Sutriani Mahalini, SpA

Aims:



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

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

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

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

prophylaxis)

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

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

There are two main clinical forms: Simple febrile seizure are a short generalized seizure, of a duration lasting than 15 minutes, not recurring within 24 hours, occurring during a febrile episode, not caused by an acute disease of the nervous system. Simple febrile seizures usually occurring during the first 24 hours of a febrile illness. Majority (70-75%) of FS are simple febrile seizure. Complex febrile seizure are a focal, or generalized and prolonged seizure, of a duration of greater than 15 minutes, recurring more than once in 24 hours, and/or associated with post-ictal neurologic abnormalities, more frequently a post ictal palsy (Todd’s palsy), or with previous neurologic deficits (American Academy of Pediatrics 1996; Berg & Shinnar, 1996; Knudsen, 2000).

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

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



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

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

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

ScenariosCase 1

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

Learning task1. What is the diagnosis and differential diagnosis? Explains the reason of your answers?2. What are the risk factor that you have to know?3. Explain possible causes of the acute seizure?4. What are the necessary diagnosis work up to support your diagnosis?5. What are the management at emergency unit? 6. Should the patient hospitalized? Explain the reasons of your answer!7. Explain long term management to the patient!8. What are information and education that should be you done?

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

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



8. What are information and education that should be you done?

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

EPILEPSY AND STATUS EPILEPTICUSDr. dr. DPG Purwa Samatra, Sp.S(K):

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

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

of anti epileptic drugs (AEDs),

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

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

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

]

Pathophysiology of seizures is underlying of abnormality between inhibition and excitatory neurotransmitters. Less of inhibition or over of excytatory neurotransmitter may be causes. In



the figure less of inhibitory neurotransmitter (GABA gamma amino butyric acid ) and over of the excitatory neurotransmitters (Glutamate) may be causes of the seizures.

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

Diagnosis of epilepsy is essentially by a clinical features. Although investigation as EEG, Brain-scan and MRI may provide assistance. The diagnosis of epilepsy is made largely on the basis of the clinical history.The drug treatment of epileptic patients has improved over recent years. There is much understanding of the principles of effective drug treatment with Anti Epileptic Drugs (AED). Practice point to manage patient with epilepsy is : Drugs treatment should be instituted only if the diagnosis of epilepsy is firm. Monotheray should be the role in the initial treatment of epilepsy and all drugs should be stated at low dosage, and built up over a period of weeks.

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

Trigger/Scenario.

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

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

Self assessment1. Describe the function of neurotransmitters.



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

Disscusion in groupsWhere the TOPICAL DIAGNOSIS in patient with :

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

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

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

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

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

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

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

DAY 3rd and 4th April 13th&14th2015HEADACHE (TENSION TYPE HEADACHE, CLUSTER HEADACHE AND MIGRAIN) AND TRIGEMINALNEURALGIAdr.Made Oka Adnyana, SpS(K)

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

Learning outcome;1. To describe the definitionof headache.2. To describe the pathophysiology of headache,3. To defrentiate primary and secondary of headache.



4. To diagnosis primary headaches (tension type headache, migraine and cluster headache).5. How to manage primary headache ( pharmacology , non pharmacology), and trigeminal neuralgia

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

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

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

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

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

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

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

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

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

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

3rd. case.



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

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

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

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

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

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

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

NEUROIMAGINGdr. Made Widhi Asih, Sp.Rad

Self Assesment :1. At emergency case, the advanced radiology modality that should be choosen is :

a. Skull fotob. Waters c. Head CT Scand. Head MRI e. PET Scan

2. For the suspicious of the thoracolumbal intra dural SOL, conventional radiology that using contrast agent is called :

a. Hysterosalphyngographyb. Intra venous pyelographyc. Caudographyd. Fistulographye. Urethrography

3. At new born neonatal with convulsion and history of manual labor, the radiology modality that most safe for baby is :



a. Cranial Ultrasonografi b. Skull fotoc. Head MRId. Head CT Scane. Caudography

Learning Task :1. A 28 year-old male patient came with paraparesa inferior since 2 weeks ago, accompanied with

lump on the upper back. a. Mention about conventional radiology examination that you suggest for this patientb. Mention about advanced radiology examination that should be done c. What is radiology findings that you will might be found

2. A 65 year-old male patient with history of hypertension, was brought by his family to the emergency department with complain of sudden weakness of his left upper and inferior extremities

a. What is diagnosis that you suspect for this patient ?b. What is the most appropriate radiological examination that suggest ?c. Explain about radiological findings that you can see in that examination

3. A 9 year-old girl patient came to hospital with chief complain fever since 3 days ago accompanied with convulsion

a. What is the radiological examination that can be choosed for this patient ?d. What is diagnosis that you suspect for this patient ?e. Explain about radiological findings that you can see in that examination

4. A 44 year-old female patient with low back pain that reffered to the left leg, and numbness on her leg, came to the hospital

a. What kind of position that should you suggest for conventional radiology, especially for evaluated intervertebral foramina

b. What is the next advanced radiology examination should be suggest for this patient ?c. Explain about the radiological finding that you wiil might be found

5. A young male came with chronic headache that getting worsen progressivelya. What kind of conventional radiology examination will you suggest for this patient ?b. What do you try to find out from that examination ? Mention about the signs c. What kind of advanced radiology examination you should suggest to performed, if from

conventional radiology showed abnormality?

DAY 5th April15th2014HNP AND RADICULAR SYNDROMEdr. Kumara Tini, Sp.S, FINS

Aim :Describe the the structure of lumbar spine and sacrum and understand how they normally operate. Clinical characteristic, risk factors , diagnostic work-up including history, clinical examination and treatment of Low Back Pain.

Learning outcome : 1. Know the the structure of lumbar spine and sacrum and understand how they normally operate.2. Understand and be able explain how back pain and somatic referred pain differ from radicular pain,

radiculopathy and sciatica.3. understand the lack of validity of diagnostic labels commonly applied to acute and chronic low back

pain.



4. Be able to obstain a comprenhensive history of LBP, physical examination, psychososial factor in the assessment of patients with LBP.

5. Understand the natural history of acute low back pain back pain6. Understand the use of diagnostic tool and lack of validity of conventional medical imaging in

assessment of LBP7. Understand management of LBP.8. Understand the reasons for the limited efficacy of surgical treatment of low back pain

AbstractIn the United State, low back pain (LBP) is the fifith most common reason for all physician office

visits and the second most common symptomatic reason. Low back pain is common and costly medical condition. The annual prevalence of low back pain in United States is estimated at 15% to 20 % while in Indonesia prevalence rate is 18 % ( Pain Study Club Indonesian Neurological Association survey 2002) Idiopathic low back pain is the most common cause of work-related disability for people age < 45 year in US

For most patients back symptoms are nonspecific, no evidence for radicular symptoms or underlying systemic disease. The history and physical examination usually provide clues to the rare but potentially serious cause of low back pain.

Clinician should not routinely obtain imaging or other diagnostic tests in patients with non specific low back pain. Clinician should perform diagnostic imaging and testing for patients with low back pain when severe or progressive neurologic deficit are present or when serious underlying conditions are suspected on the basis of history and physical examination.

Many therapeutic options are available for patients low back pain. The primary of treatment shoud be conservative care and operative. Conservative care consist of pharmacologic and non pharmacologic therapies. Clinicians should consider the use of medication with proven benefits in conjuction with back care information. For patients who do not improve with self care options, clinician should consider the addition of non pharmacologic therapy with profen benefit for low back pain. Surgical intervention decision should be made carefully because surgery doesnot tend to lead to huge improvements on average.

Self assesment.1. What is the classification of LBP ?2. What is the meaning of red flag and yellow flag ?1. Explain the mechanism herniated disc !2. Explain the diagnostic work-up LBP !

Scenario :A 45 years old man, farmer complaint low back pain suddenly after worked in this rice field . The pain is sharp pain accompanied by paresthesia that spreading to the left lateral side of thigh untill toe. There were no micturation and defection disturbances.

Learning task :1. What is the differential diagnosis of this patient ?2. If etiology of LBP in this patient is HNP (hernia nukleus pulposus) L5-S1, what is the symptoms

and signs ? what is diagnostic work-up for this patients ?3. What is the management of Lumbar HNP ?

Learning Resources :1. Atlas SJ, Deyo RA. Evaluating and Managing Acute Low Back Pain in the Primary Care Setting. J

Gen Intern Med 2001 : 16 : 120-1312. Deyo RA. Evaluating and Managing Acute Low Back Pain in the Primary Care Setting.J Gen

Intern Med. 2001 : 16 :120-131.



3. Chou R, Qaseem A, Snow V, Casey D, Cross TJ ,Shekelle P, Owens DK. Diagnosis and Treatment of Low Back Pain: A Joint Clinical Practice Guideline from the American College of Physicians and the American Pain Society. Ann Intern Med.2007 ; 47: 478-491

4. Chou R and Huffman LH. Nonpharmacologic Therapies for Acute and Chronic Low Back Pain: A Review of the Evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline. Ann Intern Med.2007 ; 47: 492-504

5. Mogil J. Pain 2010 an Updated Review. IASP Press, seattle, 2010.

NEUROGENIC BLADDERdr. Kumara Tini, Sp.S, FINS

Aim :Describe the the structure of urinary bladder and understand the normal micturation mechanism and neurogenic bladder dysfunction. Explain clinical characteristic, risk factors , diagnostic work-up including history, clinical examination and treatment of neurogenic bladder.

Learning outcome : 1. Know the the structure of urinary bladder and understand how they normally operate to control

of micturition (urination)2. Understand and be able explain that impairs bladder and bladder outlet afferent and efferent

signaling can cause neurogenic bladder.3. Understand and be able explain pathophysiology of neurogenic bladder.4. Be able to obstain a comprenhensive history, physical examination and assessment of patients

with neurogenic bladder.5. Understand management of neurogenic bladder.

AbstractNeurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a

dysfunction of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition (urination).

Symptoms of neurogenic bladder range from detrusor underactivity to overactivity, depending on the site of neurologic insult. The urinary sphincter also may be affected, resulting in sphincter underactivity or overactivity and loss of coordination with bladder function. Urinary incontinence, characterized by either the involuntary release of large volumes of urine or continuous dribbling of small amounts, bed-wetting may occur, frequent urination, Persistent urge to urinate despite recent voiding; constant feeling that the bladder is not completely empty, pain or burning on urination and dribbling urine stream

The appropriate therapy and a successful outcome are predicated upon accurate diagnosis through a careful medical and voiding history together with a variety of clinical examinations, including urodynamics and selective radiographic imaging studies.

Self assesment.1. What is the classification of neurogenic bladder ?2. What is causes of neurogenic bladder ?3. Explain the mechanism neurogenic bladder?4. Explain the diagnostic work-up neurogenic bladder?5. Explain the treatment of neurogenic bladder

Scenario :



A 55 years old man, fisherman complaint urinary retention, accompanied by a dribbling urinary stream and sexual dysfunction since 3 months ago. He has been suffering diabetes for 15 years with poorly control of blood sugar.

Learning task :1. What is the differential diagnosis of this patient ?2. what is diagnostic work-up for this patients ?3. What is the management of this patient ?

Learning Resources :1. Wein AJ, Rackley RR. Overactive bladder: a better understanding of pathophysiology, diagnosis

and management. J Urol. Mar 2006;175(3 Pt 2):S5-10. [Medline]

2. Rackley, RR, Kim, ED. Neurogenic bladder. Avaiable at http://emedicine.medscape.com/article/453539-overview accessed 11 April 2014

3. Wein AJ, Dmochowski RR. Neuromuscular dysfunction of the lower urinary tract. In: Wein AJ, Kavoussi LR, Novick AC, et al, eds. Campbell-Walsh Urology. 10th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 65.

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

AimsDescribe mechanism and function of pain

Learning OutcomesApply its concepts and principles in acute pain patient setting

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

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



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

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

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

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

DAY 6th April 16th 2015DEMENTIA / ALZHEIMERdr. I Putu Eka Widyadharma, M.Sc, SpS(K)

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

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



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

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

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

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

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

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

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

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

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

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

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

Scenario 2 :



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

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

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

MOVEMENT DISORDERS/NEUROGERIATRICdr. IA Sri Wijayanti, M.Biomed, Sp.S

Movement disorders are commom in clinical practice. Movement disorders are doe to primary and secondary. But the most populer movement disorders divided , based on movement type. Based on these movement disorders divided : hyperkinetic movement disorders and hypokinetic movement disorders.Hypokinetic : Parkinsonism Stiff-man syndromeHyperkinetic : Chorea Myoclonus Dystoniia Tics Tremor

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

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

Diagnostic criteria of Parkinsonism1. Tremor at arest2. Bradykinesia3. Rigidity4. Loss of postural reflexes5. Flexed posture6. Freezing ( motor blocks)

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



Etiologi : Common causes of Parkinsonism :

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

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

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

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

locomotion and facial expression.2. Stage two

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

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

standing3. Generalized dysfunction that is moderately severe

4. Stage four1. Severe symptoms2. Can still walk to a limited extent3. Rigidity and bradykinesia4. No longer able to live alone5. Tremor may be less than earlier stages

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

TreatmentTreatment of Parkinsonism :

1. Medical treatment2. Surgical treatment/ invasive treatment



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

inhibitor( catechol-O methyltransferase inhibitor : entacapone), type B MAO inhibitor (selegiline).2. Dopamine agonist : pramifeksole3. Anti cholenergic : trihexyphenidyl

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

Rehabilitation: Physical, accupational.

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

Hallet

DAY 7th April 17th 2015NEUROPATHIC PAIN AND NEUROPATHYdr. I Putu Eka Widyadharma, M.Sc, SpS(K)

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

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

Learning outcome1. Definition

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

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

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

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

treatment with chemotherapeutic agents.3. Etiology.

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

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

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

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

- Know the common signs associated with neuropathic pain including positive (mechanical and thermal allodynia and hyperalgesia, temporal and spatial summation), negative ( sensory loss,



weakness and muscle atrophy) and other signs ( neuroma signs, referred sensation, swelling, skin flare and discoloration, hyperhidrosis and trophic changes).

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

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

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

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

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

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

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

Diagnostic work-up including collection of medical history, focused at exploring the onset of pain and posssible association with current diseases, trauma, surgery etc.Therapeutic intervention applied in neuropathic pain consist of pharmacological and non pharmacological approach.Common pharmacological approaches used for neuropathic pain including : sodium and calcium channel blocker, NMDA receptor blocker, anti depressant, anti convulsant and opioid. NSAID is not responsive for treatment neuropathic pain.

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

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



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

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

CARPAL TUNNEL SYNDROME (CTS), TARSAL TUNNEL SYNDROME AND PERONEAL PALSYdr. I Putu Eka Widyadharma, M.Sc, SpS(K)

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

Learning outcome:1. To Describe the definition of CTS, TTS AND PERONEAL PALSY2. To describe patophysiology of CTS, TTS AND PERONEAL PALSY3. To describe diagnosis and differential diagnosis of CTS, TTS AND PERONEAL PALSY4. To describe how to manage CTS, TTS AND PERONEAL PALSY

Curiculum contens:1. Epidemiology of CTS, TTS AND PERONEAL PALSY2. Clinical presentation of CTS, TTS AND PERONEAL PALSY3. Risk factor of CTS, TTS AND PERONEAL PALSY4. Pathophysiology of CTS, TTS AND PERONEAL PALSY5. Diagnosis and Differential diagnosis of CTS, TTS AND PERONEAL PALSY6. Treatment of CTS, TTS AND PERONEAL PALSY

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

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

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

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

Self assesment.



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

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

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

DAY 8th May 26th2014CENTRAL NERVOUS SYSTEM TUMORdr. Made Susilawathi, Sp.S

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

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

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

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

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



8. How to manage of the brain tumour ?9. How is the prognose of the brain tumour ?

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

involved4. Student be able to explain diagnostic tool to assess brain and spine tumour5. Student be able to explain how to manage the basic treatment of brain and spine tumour6. Student be able to explain when to refer patient with headache which is suspected brain

tumour

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

Aims:To understand traumatic brain injury

Learning Outcome1. Comprehend the specific principles of anatomy and physiology related to brain injury.2. Identify and discuss the principles of general management of unconscious patient.3. Outline the method of evaluating head injury using a minineurologic examination 4. Identify and discuss the management techniques of head injury.

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

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

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

Neurotrauma



Clinical factors adversely influencing outcome [death and disability] - Severity of Primary Injury- Intracranial Complications- Hypoxaemia- Hypercarbia- Hypotension- Anaemia- Multiple Injuries- Age- Prolonged Prehospital Time- Admission To Inappropriate Hospital- Delayed Or Inappropriate Interhospital Transfer/ Retrieval- Delay In Definitive Surgical Treatment

Learning TaskHead Injury

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

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

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

DAY 9th May 28th2014STROKEdr. AABN. Nuartha, Sp.S(K):

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

Learning outcome:



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

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

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

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

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

Learning Task1. Pathogenesis of stroke.2. Clinical aspect and diagnostic tool of stroke3. Management and prevention of stroke.

SURGICAL ASPECT OF CEREBROVASCULAR ACCIDENTS (CVA)dr. I Wayan Niryana, M.Kes, SpBS(K)



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

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

CURRICULUM CONTENTS:Cerebrovascular Accidents (CVA)

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

ABSTRACTS OF LECTURES

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

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

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

Etiology: There are two categories, primary and secondary.

PrimaryICH:It is associated with hypertension and distinct from hemorrhagic infarcts. It has been suggested that hypertensive changes in the arterial wall, such as, hyaline degeneration, and micro aneurysms are at fault. Another suggestion is the thin walled vessels (such as lenticulostriates), originating directly from the main vessel are subjected to higher intravascular pressure than the cortical vessels and tend to rupture.Eighty percent of them are supratentorial.



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



Coagulation studies must be done as a routine in addition to ECG, chest X-ray and other general investigations.Management: Supportive care control of hypertension, reduction of ICP without compromising the CPP and prevention of complications are the mainstay. Fluid and electrolytes and tissue oxygenation must be closely monitored. The aim is to avoid secondary events.An aggressive decrease of high BP may lead to cerebral ischemia. Ideally, it should not be lowered below 150mm Hg systolic and 100 mm of Hg diastolic. Should general measures to control the raising ICP fail, hyperventilation may help; but must be employed with careful watch on pCo2, arterial blood pressure and preferably with ICP monitoring as well. The CPP should not be compromised. Osmotherapy with mannitol may help only when the serum osmolality is lower than 300 mosm/kg.Prophylactic anti convulsant therapy is advised by most physicians with no supporting evidence. The role of surgical intervention is controversial. Neurosurgeons and neurologistsadvocate that large cerebellar hemorrhages with compressionof the brain stem or obstruction of the fourth ventricle shouldbe surgically removed as soon as possible. Surgical removalof large lobar hemorrhages in young patients who are clinicallydeteriorating has also been recommended based on anecdotal experience. On the other hand, the results of such surgery in hematomas within the basal ganglia and other deep structures are unacceptable. Standard craniotomy for surgical removal of primary brainstem or thalamic hemorrhages has been all but abandoned becauseof the extremely poor outcomes in almost all patients.Craniotomy: Craniotomy and evacuation of the clot has been the standard approach for removal of intraparenchymal hemorrhage. In addition a decompressive craniectomy with a duraplasty is preferred by some.Its major advantage is adequate exposure to remove the clot. It is not difficult or time-consuming. The major disadvantageof a more extensive surgical approach is that it may lead tofurther brain damage, particularly in patients with deep-seated hemorrhages.In addition, the effectiveness of clot removal by craniotomyis far from ideal.There have been numerous nonrandomized series comparing craniotomy and bestmedical treatment of ICH. Recently Morgenstern and colleagues reported a single-center, randomized trial (STICH Trial) ofstandard craniotomy versus best medical therapy in patientswithsupratentorial ICH; the goal was to perform surgery 12 hours after symptomonset. Patients had to have a supratentorial ICH with a volume10 cm3 and a GCS score of 5 to 15. Of the 34 patients in therandomized trial, 17 were randomized to removal of the ICH bystandard craniotomy. The median time to surgery for the 17 patientswas 8.3 hours (minimum 3.75 hours and maximum 26.1 hours). The6-month mortality for the surgical group was 17.6% comparedwith 23.5% for the medical group. The median 6-monthBarthel index score for survivors in the surgical group wasalso similar to the median Barthel index score for the medicalgroup. However, the groups were not balanced with regard to ICHlocation. Only 1 of the 17 patients (6%) in the surgical grouphad a lobar hemorrhage compared with 7 of 17 patients (41%)of the medical group.Nonrandomized treatment series of patients with cerebellar hemorrhagereport good outcomes for surgically treated patients who havelarge (>3 cm) cerebellarhemorrhages or cerebellar hemorrhageswith brain stem compression or hydrocephalus. Inthese patients, medical management alone often results in badoutcomes. Smaller cerebellar hemorrhages without brain stemcompression that are managed medically do reasonably well.Outcome: The natural course of spontaneous ICH leads to a 30-day mortality rate of 45% . The patient's initial level of consciousness, hemorrhage size, and intraventricular extension of blood has proven to be accurate predictors of outcome. Less commonly, age, sex, hypertension, and mass effect may indicate harmful effects on outcome in patients with ICH.

The author recommends that patients with smaller hematomas who are alert, stable, or improving should be treated medically and the patients with larger hematomas who show progressive neurological deficit, prolonged functional impairment, and intracranial hypertension should be treated surgically.



Patientswith a GCS score <4 should also be treated medically because theyuniformly die or have extremely poor functional outcome that cannotbe improved by surgery. Easily accessible supratentorial hematomas with mass effect, especially in the young and in those with a GCS score >5, must be evacuated. The aim of surgery should be the removal of as much of the clot as possible, with minimal disruption of surrounding brain tissue. If possible,surgery should also remove the underlying cause of hemorrhage, suchas an arteriovenous malformation, and prevent complicationsof ICH such as hydrocephalus and mass effect of the blood clot. Morecomplete clot removal may decrease elevated ICP and local pressure effectsof the blood clot on the surrounding brain. Stereotacticaspiration may be associated with better outcomes than standardcraniotomy; but thishypothesis has yet to be tested in a randomized study. Ultra-earlyremoval of ICH by localized, minimally invasive surgical proceduresis promising but untested. Further study of the dynamics of hemorrhage and additional results are needed prior to making a decision on how to divide patient management into the two categories of surgical and nonsurgical treatment.

SCENARIOMale patient, 50 years oldwas referred to the Emergency room on a face mask oxygenation, with

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

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

SELF ASSESMENT

1. Explain the Cerebrovascular Anatomy that supplies the brain and cerebellum.2. Learn about clinical features, investigations and differentials diagnosis of cerebrovascular disease.3. Learn about emergency management: medical and surgical aspect of CVA.4. Learn about how to explain the prognosis of CVA.

DAY 10th June 2nd2014SPINAL CORD INJURY, COMPLETE SPINAL TRANSECTION, ACUTE MEDULLA COMPRESSIONDr. dr. Tjokorda GB Mahadewa, M.Kes, Sp.BS(K)Spinal

SPINAL CORD INJURYAims:Provide initial assessment and management, established tentative diagnosis, proposed definitive management, and rehabilitation method or refer patient with Spine and Spinal Cord Injury



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

Curriculum contents:Spine and Spinal Cord Injury:

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

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

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

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

Emergency actionsUrgent medical attention is critical to minimizing the long-term effects of any head or neck trauma. So treatment for a spinal cord injury often begins at the scene of the accident. If you suffer a head or neck injury, you'll likely be treated by paramedics and emergency workers who will attend to three immediate concerns:

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

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



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

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

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

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

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

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

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

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

driver was died immediately at the scene. The patient was referred to the Emergency room as being immobilized on a long spine board and semirigid cervical collar. On a face mask oxygenation, with Infusion lines at both arms with large caliber of needles, warmed crystalloids has been administered. The blood pressure is 85/40 mmHg, heart rate 130x/mnt, Respiration rate 40x/mnt, shallow respiration pattern, with



an obvious injury on the chest wall. His eyes are open and well respond to verbal stimuli. He can lift up his shoulder but cannot elevate his elbows neither his legs.

6. What is the working diagnosis?7. How is the prompt management for this patient?8. How should you explain the prognosis of the patient to the family?

Learning tasks5. Learn about Initial Assessment and Management for Spinal Injury.6. Learn about Spinal Injury diagnosis and management for Spinal Injury.7. Learn about rehabilitation methods for Spinal Injury.8. Learn about how to refer patient with Spinal Injury

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

POST TRAUMATIC AMNESIAdr. IGN Budiarsa, Sp.S

Aim:Describe the patophysiology, epidemiology, clinical finding, diagnostic work-up and treatment of post traumatic amnesia.

Learning outcome:1. Understanding the patophysiology mechanism of post traumatic amnesia.

Post traumatic amnesiais the inability to recall events that are taking place, after experiencing trauma in the head which causes a change in consciousness.

2. Recognize the epidemiology of post traumatic amnesia.In 6% of cases, post-traumatic amnesia took less than one hour; 7% of it, experienced memory loss for an hour for a day; 16 % of it, lasted for several days and weeks; 23 % of it, lasted within a weekly and monthly, and 45 % of it, had amnesia for more than a month.

3. Know the clinical presentation of post traumatic amnesia.4. Be able to make work-up including clinical finding and another comprehensive test.5. Understanding the management of post traumatic amnesia.

AbstractPost traumatic amnesiais the inability to recall events that are taking place, after experiencing

trauma in the head which causes a change in consciousness. Post traumatic amnesiais a term that was first used in 1928 by Symonds which is a period from the occurrences of head injuries until the patient is fully conscious again. The impaired memory is a memory about events that are taking place, including the event in where the patient is unconscious.

A case study on head injuries shows that less than 3% of it did not experience memory loss at all. In 6% of cases, post-traumatic amnesia took less than one hour; 7% of it, experienced memory loss for an hour for a day; 16 % of it, lasted for several days and weeks; 23 % of it, lasted within a weekly and monthly, and 45 % of it, had amnesia for more than a month.

Memory is stored as a short-term memory. Short-term memory is a memory that persists within seconds to hours. Long-term memory can last a few days, years, even a lifetime. The process of changing from short-term memory into long-term memory is called consolidation process. During consolidation, short-term memory is activated repeatedly, so much so that there is a change of certain chemical substances and physical changes in the brain which causes a permanent memory or "embedding"



permanently for long-term access. If something disturbing happens during the reactivation process, for example, concussions or other brain trauma, then the short-term memory cannot consolidate. Later, the memory cannot be stored for long-term access. This might occur in anterograde amnesia. The consolidation process takes place in the hippocampi which located in the temporal lobe of the brain. If the hippocampi are damaged, the patient will be able to recall an old memory, but will not be able to remember a new a memory. More severe trauma can also disrupt long-term memory.

During post-traumatic amnesia, the patient's consciousness is called "clouded". In addition to memory loss in posttraumatic amnesia, patients also experience confusion; so, "posttraumatic confusional state" term can be used as an alternative. During this period, individuals may experience the following events:

- Confusion: confused about where they are, who are the people around them and the time, date or year.

- Impaired concentration.- Having difficulty with ideas, memory and concentration.- They may be scared, anxious and emotionally unstable.

Symptoms of post traumatic amnesia can be categorized as follows:- Anterograde Amnesia

Is a form of amnesia in where a person is unable to remember events or new events in short-term memory because it is not transferred as a permanent long-term memory. In anterograde amnesia, what happens is the inability to save memory on the long-term storage for later reissued. This amnesia is usually associated with damage to the temporal part of the brain which responsible for consolidation. People who suffer from this type of amnesia can remember what they learned before the amnesia, but they cannot save new memory permanently.

- Retrograde AmnesiaIs a form of amnesia where a person cannot remember events that occurred before suffering amnesia. It is more than a usual forgetting event. This type of amnesia is defined as "a loss of some or all of the ability to recall events that had occurred during the period prior to the brain injury."

Both categories of amnesia can occur simultaneously on a person, and usually is as a result of the influence of drugs or damage to the medial temporal lobe regions, particularly hipocampus. Diagnostic work-up is anamnesis, physical examination, and other examinations, for example:

- When doing anamnesis, note the general appearance of the patient; behavior, expression, and the thought of patient. Physical examination includes examination of the patient's vital signs and level of consciousness value. Check the right and left pupils, both of the pupils should be equal in size and should miosis quickly when exposed to direct light. Assess the second movement of his eyes as well. Check the motor function by asking the patient to move his hands and legs. Check for physiological and pathological reflexes. To examine short-term memory patients, doctors may ask patients to identify and name three types of objects. Then repeat it again after 3 minutes. To examine the intermediate memory, it can be asked with the question: "Who is the president of Indonesia before the current period?" and "What kind of car or motorcycle which is your last purchased?” To examine the long-term memory, it can be asked with a question such as the following, "How old are you?" and "Where were you born?"

- Supporting examinations which may be conducted is Magnetic Resonance Imaging (MRI), Computerized Tomography (CT) and Electroencephalogram (EEG). From this examination, the presence or absence of damage or abnormalities in the brain can be determined.

- Complete blood lab tests may be done to assess the presence of infection, nutritional deficiencies or other problems.



Treatment for the amnesia disorder is to treat the basic cause of amnesia. The basic principle of handling head injury, namely:

- Monitor the intracranial pressure and decline of it.- 30 degrees head elevation.- Medical treatment to decrease brain edema.- Decreased brain activity, decrease oxygen delivery to the induction of coma.- Surgical decompression.- Prophylactic therapy against seizures.

Self-assessment1. Explain the patophysiology of post traumatic amnesia2. Explain the clinical presentation of post traumatic amnesia3. Describe the diagnostic work up for post traumatic amnesia4. Describe the medications approaches for post traumatic amnesia

Scenario:40 years old male had a motorcycle accident. When the patient comes to the hospital, the patient’s consciousness is good, but when anamnesis, the patient is unable to remember events when he was riding his motorcycle because of the head injury and he did not remember the incident at the hospital two days after the head injury.

Learning task:1. What is the diagnostic of this patient?2. What is another diagnostic work up for this patient?3. What is the management planned for thus patient?

Learning resources:1. Ropper, A, Brown, R. 2009. Adams and Victor’s: Principles of Neurology. 9th ed. New York:

McGraw-Hill. p.376-383.2. Robert C.Cantu. 2001. Post traumatic Retrograde and Anterograde Amnesia: Pathophysiology and

implications in Grading and safe return to play. p.244-248.

DAY 11th June 3rd 2014GULLAIN BARRE SYNDROME AND MYASTENIA GRAFIS dr. IGN Budiarsa, Sp.S

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

and prognosis of Guillan-Barre Syndrome (GBS).

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

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

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

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

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

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

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

7th ed. New York: Oxford University Press.

ENSEFALOPATI, 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 coma2. Able to locate the pathology of coma

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

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

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

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

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

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

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

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

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

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

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

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

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



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

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

Learning resources:1. 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.2. Longmore M, Wilkinson I, Turmezei T, Cheung CK. 2007. Oxford Handbook of Clinical Medicine.

7th ed. New York: Oxford University Press.

DAY 12th June 4th 2014CENTRAL NERVOUS SYSTEM (CNS) INFECTIONS (1): MENINGITIS, ENSEFALITIS, MALARIA SEREBRAL, RABIESdr. Ni Made Susilawathi, Sp.S

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

Learning Outcome:

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

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

3. Describe Manifestation HIV infection in Nervous System including:a. Encephalopathyb. Myelopathyc. Neuropathy

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



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

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

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

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

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

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

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

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

Self Directing LearningBasic knowledge that must be known:

1. The Meningens and The cerebrospinal fluid and ventricular system 2. The technique performing a lumbar puncture/spinal tap3. Cerebrospinal fluid finding in CNS infection

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 380C , Blood pressure 110/68 mmHg and pulse 100 beat/min. His neurologic examination is notable for kernig sign and hyperreflexia.

Learning Task:

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

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

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

CENTRAL NERVOUS SYSTEM (CNS) INFECTIONS (2): CNS HIV/AIDS, POLIOMIELITIS, TETANUS, TETANUS NEONATORUMdr. D.K. Indrasari Utami, Sp.S

Tetanus is an acute disease caused by an exotoxin of bacterium Clostridium tetani. The etiology discovered by Carle and Rattone in 1884. The Clostridium tetani is sensitive to heat and can not survive in the presence of oxygen. The spores of Costridium tetani are distributed in soil and in the intestine and feces of dogs, cats, pigs, chickens, sheep, horses and rats. C. tetani produced two exotoxins i.e tetanospasmin and tetanolysin.

The incubation period is about 8 days (range 3 to 21 days). Anaerobic conditions allow germination of spores and production of toxins. Tetanus is characterized by muscle spasm, initially in the jaw muscle. There are three different forms of tetanus : local tetanus, cephalic tetanus, and generalized tetanus. Tetanus is often fatal and cause death. The complications of tetanus are otonom disfunction, respiratory problem, renal and electrolyte dysfunction, and nosocomial infection. The medical management of tetanus are : all wounds should be cleaned, eradication of causative bacterial, remove unbound tetanus toxin, supportive therapy, and immunization.

Refferences :1. World Health Organization (WHO), 20142. Centers for Diseases Control and Prevention (CDC), 20133. Dian S., Tetanus., 2011., Infeksi pada Sistim Saraf., Kelompok Studi Neuro Infeksi, Perdossi4. Prof.dr. I Gst. Ng. Gd. Ngoerah; 1991; Dasar-Dasar Ilmu Penyakit Saraf; Airlangga University

Press

Case :A 49 year-old man just arrived at the hospital with chief complain can’t open his mouth since yesterday.

Learninng task :1. Please do the complete anamnesis to this patient2. What is your differential diagnosis? Why?



3. What should you do to get the diagnosis?4. How to manage the patient?

Self Asssessment :1. Learn about the clinical feature of tetanus2. Learn the pathogenesis of tetanus3. Learn the wound management 4. Learn about immunization for tetanus

POLIOMYELITISdr. D.K. Indrasari Utami, Sp.S

Poliomyelitis (polio) is mainly affects young children. Poliomyelitis caused by a virus that invades the nervous system, and can spread from person to person. There is no cure but preventable by safe and effective vaccines.

Most of persons who infected with polio will have no symptoms (approximately 72%), about 24% have minor symptoms. The minor symptoms are : fever, headache, fatique, flu-like symptoms, nausea, neck and back stiffness, pain in the limbs, which can resolve completely. Only less than 1% result in permanent paralysis of the limbs. When the paralysis affected the respiratory muscles, 5-10% persons infected with polio died.

Refferences :1. Centers for Diseases Control and Prevention (CDC), Global Health – Polio,20132. World Health Organization (WHO), Poliomyelitis (Polio), 20143. Prof.dr. I Gst. Ng. Gd. Ngoerah; 1991; Dasar-Dasar Ilmu Penyakit Saraf; Airlangga University

Press

Case :A 5 years old child, come to clinic with his parents because his left leg paralyzed since two days ago. There is no pain or numbness on the leg.

Learning task :1. Please do the complete anamnesis to this patient2. What is your differential diagnosis? Why?3. What should you do to get the diagnosis?4. How to manage the patient?

Self Assessment :1. Learn the anatomy of medulla spinalis and peripheral nerve2. Learn the cause of poliomyelitis3. Learn the clinical feature of poliomyelitis4. Learn the pathogenesis of poliomyelitis5. Learn the prevention of poliomyelitis

TETANUS NEONATORUMdr. D.K. Indrasari Utami, Sp.S

Tetanus neonatorum (neonatal tetanus) is a major cause of mortality in infant in underdevelop countries. Infection results from umbilical cord contamination during unsanitary delivery, and a lack of maternal immunization (the mother is not immune).



In tetanus neonatorum, symptoms usually appear from 4-14 days after birth, averaging about 7 days. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. Tetanus neonatorum is a form generalized tetanus that occurs in newborn infants without protective passive immunity. Neonatal tetanus has a very poor prognosis.

Neonatal tetanus can be prevented by immunizing women of childbearing age with tetanus toxoid, either during pregnancy or outside of pregnancy.

Refferences :1. Patrick B Hinfey, MD; Tetanus ; Mar 2014 ; Medscape 2. World Health Organization (WHO), 20083. Centers for Diseases Control and Prevention (CDC), 2013

Case :A 14 days baby just arrived at the hospital with chief complain irritable, feed poorly, and develop rigidity with spasms since 3 days ago.

Learninng task :1. Please do the complete anamnesis to this patient2. What is your differential diagnosis? Why?3. What should you do to get the diagnosis?4. How to manage the patient?

Self Assessment :1. Learn about the clinical feature of tetanus2. Learn the pathogenesis of tetanus neonatorum3. Learn the management 4. Learn about immunization for tetanus prevention



~ CURRICULUM MAP ~Smstr Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerkship

7

Medical Emergency(3 weeks)

BCS (1 weeks)

Special Topic:-Travel medicine(2 weeks)

Elective Study III(6 weeks)

Clinic Orientation (Clerkship)(6 weeks)

6

The Respiratory System and Disorders(4 weeks)

BCS (1 weeks)

The Cardiovascular System and Disorders(4 weeks)

BCS (1 weeks)

The Urinary System and Disorders(3 weeks)

BCS (1 weeks)

The Reproductive System and Disorders(3 weeks)

BCS (1 weeks)

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-Complementary & Alternative Medicine- Forensic(3 weeks)

Elective Study II(1 weeks)

4Musculoskeletalsystem &connectivetissue disorders(4 weeks)

Neuroscienceandneurologicaldisorders(4 weeks)

Behavior Changeand disorders(4 weeks)

The Visualsystem &disorders(2 weeks)



BCS (1 weeks) BCS (1 weeks) BCS(1 weeks)BCS(1 weeks)

3

Hematologicsystem & disor-ders & clinicaloncology(4 weeks)

BCS (1 weeks)

Immunesystem &disorders(2 weeks)

BCS(1 weeks)

Infection& infectiousdiseases(5 weeks)

BCS (1 weeks)

The skin & hearing system& disorders(3 weeks)

BCS(1 weeks)

2

Medical Professionalism(2 weeks)

BCS (1 weeks)

Evidence-based Medical Practice(2 weeks)

Health System-based Practice(3 weeks)

BCS (1 weeks)

Community-based practice(4 weeks)

Special Topic- Ergonomi- Geriatri(2 weeks)

Elective Study I(2 weeks)

1

StudiumGenerale and Humaniora(3 weeks)

Medicalcommunication(3 weeks)

BCS (1 weeks)

The cellas bioche-mical machinery(3 weeks)

BCS(1 weeks)

Growth&development(4 weeks)

BCS: (1 weeks)

Pendidikan Pancasila & Kewarganegaraan (3 weeks)


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