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STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS

Planners

IA Sri Wijayanti Putu Gede Sudira Ni Putu Sriwidyani Anna Marita Gelgel Kumara Tini

Ketut Widyastuti

IA Sri Indrayani Ni Made Susilawathi Ni Putu Witari Sri Maliawan

Dewi Sutriani Mahalini

Contributors

I Nyoman Mangku Karmaya D.A. Inten Dwi Primayanti I Wayan Sugiritama I Made Jawi

Ni Putu Sriwidyani I Nyoman Wande DPG Purwa Samatra I Made Oka Adnyana IGN Budiarsa

Thomas Eko Purwata AAA Putri Laksmidewi Anna Marita Gelgel Kumara Tini

IB Kusuma Putra

I Komang Arimbawa Putu Pramana Ketut Widyastuti IA Sri Indrayani Ni Made Susilawathi Ni Putu Witari Sri Maliawan Nyoman Golden

Tjokorda GB Mahadewa I Wayan Niryana

Dewi Sutriani Mahalini Made Widhi Asih IA Sri Wijayanti Putu Gede Sudira Editors

Putu Gede Sudira Layout

Rizky Darmawan

First Edition September 2017

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise without prior written permission of the publisher.

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CONTENTS

STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS ... 2

CONTENTS... 3

PREFACE ... 5

CURRICULUM MAP... 6

GENERAL CURRICULUM OF NEUROSCIENCE AND NERVUS SYSTEM DISORDERS ... 7

PLANNERS AND LECTURERS ... 13

FACILITATORS ... 14

LEARNING ACTIVITY ... 15

IMPORTANT INFORMATIONS ... 15

STUDENT PROJECT ... 16

ARTICLE REVIEW ASSESSMENT FORM ... 18

ARTICLE REVIEW ASSESSMENT FORM ... 19

SELF ASSESSMENT ... 20

ASSESSMENT METHOD ... 20

GENERAL TIME TABLE FOR A AND B CLASSES ... 20

TIME TABLE OF CLASSES ... 21

LEARNING PROGRAMS ... 29

LECTURE 1... 29

LECTURE 2... 32

LECTURE 3... 34

LECTURE 4... 37

LECTURE 5... 40

LECTURE 6... 42

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LECTURE 13-14 ... 69

LECTURE 15 ... 71

LECTURE 16 ... 73

LECTURE 17 ... 75

LECTURE 18 ... 80

LECTURE 19 - 20 ... 84

LECTURE 21 ... 86

LECTURE 22 -23 ... 91

LECTURE 24 ... 94

LECTURE 25 ... 98

LECTURE 26 ... 100

LECTURE 27 ... 102

LECTURE 28 ... 104

LECTURE 29 ... 107

LECTURE 30 ... 114

LECTURE 31 ... 117

LECTURE 32 ... 119

LECTURE 33 ... 121

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PREFACE

The medical curriculum has become increasingly vertically integrated, with stronger basic concept and support by clinical examples and cases to help in the understanding of the relevance of the underlying basic science. Basic science concepts may help in the understanding of the pathophysiology and treatment of diseases. Neuroscience and nervus system disorders block has been written to take account of this trend, and to integrate core aspects of basic science, pathophysiology and treatment into a single, easy to use revision aid.

The neuroscience and nervus system disorders block will refresh neuroscience of basic anatomy, histology, physiology of human neurological system, pharmacology of different classes of nervus system related drugs, symptom and signs of major neurological diseases and its pathophysiology and basic principle concept to education, prevention, treatment and rehabilitation in nervus system disorders in patient, family and community. This study guide is developed by the academic staffs from various departments: Anatomy, Physiology, Histology, Pharmacology, Anatomy and Clinical Pathology, Neurology, Pediatric Neurology, Aneshtesiology, Neurosurgery and Radiology.

The learning process will be carried out for 3 weeks (15 working days) and 1 week for Basic Clinical Skills starts from September 26th, 2017 as shown in the time table. The final

examination will be conducted on October 26th, 2017 in the form of Multiple Choice Questions.

The learning situation include lecture, individual learning, small group discussion, plenary session, practice, and clinical skills.

Most of the learning material should be learned independently and discuss in Small Group Discussion by the students with the help of facilitator. Lecture is given to emphasize the most important thing of the material. In small group discussion, the students gave learning task to lead their discussion.

This simple study guide need more revision in the future, so that the planners kindly invite readers to give any comments and critics for its completion. Thank you.

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DISORDERS

Aims:

 Comprehend the structure, physiology, and pathology of the nervus system.

 Interpret the laboratory and imaging examination of the nervus system disorders.

 Diagnose and treat the patient with common nervus system disorders.

 Plan education, prevention, management and rehabilitation of nervus system disorders to patient, family and community.

Learning outcomes:

 Concern about the size of problem and diversity of nervus disease in the community.

 Able to describe the structure and function of the nervus system.

 Able to interpret the result of examination (physical, laboratory, and imaging studies).

 Able to explore patients with nervus problem.

 Able to manage major and common nerurological diseases

 Able to implement rehabilitation of nervus diseases.

Curriculum contents:

 Structure and function of the nervus system.

 Physiology of the CNS, PNS, ANS.

 Symptoms and signs of neurological disease.

 Pathophysiology of nervus system disorders.

 Basic physical, laboratory, electrocardiography and imaging examination.

 Interpretation of examination results.

 Drugs that commonly used in nervus system disorders.

 Basic principles of education, prevention, treatment and rehabilitation in nervus system disorders in patient, family and community.

Curriculum structure:

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PLANNERS AND LECTURERS

NO NAME DEPARTMENT PHONE

1 Prof. Dr. dr. I Nyoman Mangku Karmaya, M.

Repro, PA(K) Anatomy 0811387105

2 dr. D.A. Inten Dwi Primayanti, M.Biomed Fisiology 081337761299

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

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

5 Dr. dr. Ni Putu Sriwidyani, Sp.PA Anatomy Pathology 081337115012 6 Dr. dr. I Nyoman Wande, Sp.PK Clinical Pathology 08124686885 7 Dr. dr. DPG Purwa Samatra, Sp.S(K) Neurology 08123918731 8 Dr. dr. I Made Oka Adnyana, Sp.S(K) Neurology 0817347697

9 dr. IGN Budiarsa, Sp.S Neurology 0811399673

10 Dr. dr. Thomas Eko Purwata, Sp.S(K) FAAN Neurology 08123948477 11 Dr. dr. AAA Putri Laksmidewi, Sp.S(K) Neurology 0811388818 12 Dr. dr. Anna Marita Gelgel, Sp.S(K) Neurology 08113980999

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

14 dr. IB Kusuma Putra, Sp.S Neurology 085738534259

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

16 dr. Ketut Widyastuti, Sp.S Neurology 08123634110

17 dr. Ida Ayu Sri Indrayani, Sp.S Neurology 081246751536 18 dr. Ni Made Susilawathi, Sp.S(K) Neurology 08124690137

19 dr. Ni Putu Witari, Sp.S Neurology 081338724040

20 Prof. Dr. Dr. Sri Maliawan, Sp.BS(K) Neuro-surgery 0811398466 21 Dr. dr. Nyoman Golden, Sp.BS(K) Neuro-surgery 0811380037

22 Dr. dr. Tjokorda GB Mahadewa, M.Kes, Sp.BS(K)

Spinal Neuro-surgery 0818484654

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FACILITATORS

Regular Class (Class A)

No Name Group Departement Phone (2Venue ndfloor)

1 Prof. dr. I D P Sutjana, M.Erg A1 Physiology 08123924477 2nd floor: R.2.01

2 Dr. dr. Desak Made Wihandani, M.Kes A2 Biochemistry 081338776244 2nd floor: R.2.02

3 Dr. dr. BK. Satriyasa, M.Repro A3 Pharmacology 087777790064 2nd floor: R.2.03

4 dr. I Nyoman Gede Wardana, M.Biomed A4 Anatomy 087860405625 2nd floor: R.2.04

5 dr. Luh Olivia Saraswati Suastika, Sp.JP, FIHA A5 Cardiology 081330530247 2nd floor: R.2.05

6 Dr. dr. Ni Nyoman Sri Budayanti, Sp.MK (K) A6 Microbiology 08553711398 2nd floor: R.2.06

7 dr. IGN Sri Wiryawan, M.Repro A7 Histology 082341768888 2nd floor: R.2.07

8 dr. Ni Luh Pt. Ratih Vibriyanti Karna, Sp.KK A8 Dermatovenerology 081337808844 2nd floor: R.2.08

9 dr. Ni Putu Wardani, M.Biomed, Sp.An A9 DME 08113992784 2nd floor: R.2.21

10 dr. I Ketut Mariadi, Sp.PD A10 Medicine Internal 08123853700 2nd floor: R.2.22

English Class (Class B)

No Name Group Departement Phone (2Venue ndfloor)

1 Dr. dr. I Made Sudarmaja, M.Kes B1 Parasitology 081239539945 2nd floor: R.2.01

2 dr. Pande Putu Yuli Anandasari, Sp.Rad B2 Radiology 081327941987 2nd floor: R.2.02

3 Dr. dr. I Made Jawi, M.Kes B3 Pharmacology 08179787972 2nd floor: R.2.03

4 dr. IGAB. Krisna Wibawa, Sp.B(K)V B4 Surgery 08123858698 2nd floor: R.2.04

5 dr. Putu Gede Sudira, Sp.S B5 DME 081805633997 2nd floor: R.2.05

6 dr. I Gusti Ngurah Mayun, Sp.H.K B6 Histology 081237395050 2nd floor: R.2.06

7 Dr. dr. I Wayan Weta, MS, SpGK B7 Public Health 081337005360 2nd floor: R.2.07

8 Prof. Dr. I Nyoman Adiputra, M.O.H. PFK B8 Physiology 0811397971 2nd floor: R.2.08

9 Dr. dr. I Nyoman Bayu Mahendra, Sp.OG (K) B9 Obgyn 081339550423 2nd floor: R.2.21

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LEARNING ACTIVITY

There are several types of learning activity:  Lecture

 Plenary session

 Independent learning based on the lecture’s topic

 Small group discussion to solve the learning task

 Practicing

 Student project

 Clinical skill and demonstration

 Self assessment at the end of every topic

Lecture will be held at room 4.02 (4th floor), while discussion rooms available at 2nd floor

(room 2.01-2.08, 2.21 and 2.22).

IMPORTANT INFORMATIONS

Meeting of the students’ representative

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STUDENT PROJECT

Title of student project

Group Topic Evaluator

A1 Dystonia & Sindrom Tourette’s Dr. dr. DPG Purwa Samatra, Sp.S(K) A2 Normal Pressure Hydrocephalus Dr. dr. AAA Putri Laksmidewi, Sp.S(K)

A3 Childhood Brain Tumors Dr. dr. Nyoman Golden, Sp.BS(K)

A4 Neuromyelitis Optica dr. Putu Witari, Sp.S

A5 Sindrom Tolosa Hunt Dr. dr. Made Oka Adnyana, Sp.S(K)

A6 Arteriovenous Malformation dr. I Wayan Niryana, M.Kes, Sp.BS(K)

A7 Neuronitis Vestibularis dr. Ida Ayu Sri Indrayani, Sp.S

A8 Becker’s Dystrophy dr. Dewi Sutriani Maharini, Sp.A

A9 Cerebral Angiography dr. Made Widhi Asih, Sp.Rad(K)

A10 Polymyositis dr. IA Sri Wijayanti, M.Biomed,Sp.S

B1 Subdural Haematoma Prof. Dr. dr. Sri Maliawan, Sp.BS(K)

B2 Tabes Dorsalis Dr. dr. Thomas Eko Purwata, Sp.S(K)

FAAN

B3 Brown-Sequard Syndrome Dr. dr. Tjokorda GB Mahadewa, M.Kes

Sp.BS(K)Spinal B4 Tindakan DSA Pada Stroke Iskemik dr. IGN Budiarsa, Sp.S

B5 Wallenberg Syndrome dr. IB Kusuma Putra, Sp.S

B6 Vegetative state dr. I Komang Arimbawa, Sp.S

B7 Thoracic Outlet Syndrome Dr. dr. Putu Pramana, Sp.An, KMN.,M.Kes

B8 Temporal Lobe Epilepsy Dr. dr. Anna Marita, Sp.S(K)

B9 Cytomegalovirus Encephalitis dr. Putu Gede Sudira, Sp.S

B10 Therapeutic Spinal Tap dr. Putu Gede Sudira, Sp.S

About Topic, Presentation’s place and schedules, Task rules, Assessment, and Evaluator will be discussed at lecture of block introduction on September 26th, 2017.

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TITLE

(subject/ topic: choose from compentency list)

Members’ Name and Student Registered Number

Faculty of Medicine Udayana University

2017

______________

Example: Journal

Sheetz MJ, King GL. Molecular understanding of hyperglycemia’s adverse effect for diabetic complications. JAMA. 2002;288:2579-86.

Textbook

Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D, Hoster S, Longo D, Jamason S (eds). Harrison’s principles of internal medicine. 15th ed.

New York: McGraw Hill; 2001. p. 1977-82.

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ARTICLE REVIEW ASSESSMENT FORM Faculty of Medicine, Udayana University

___________________________________________________________________________

Block : The Neuroscience and Nervus System Disorders

Name : ________________________________________

Student No. (NIM) : ________________________________________

Facilitator : ________________________________________

Title : ________________________________________

________________________________________

Time table of consultation

Point of discussion Week Date Tutor sign

1. Title 1

2. Refferences 1

3. Outline of paper 2

4. Content 3

5. Final discussion 4

Assessment

A. Paper structure : 7 8 9 10

B. Content : 7 8 9 10

C. Discussion : 7 8 9 10

Total point : ( A + B + C ) : 3 = _____________

Denpasar, ______________________

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ARTICLE REVIEW ASSESSMENT FORM Faculty of Medicine, Udayana University

___________________________________________________________________________

Block : The Neuroscience and Nervus System Disorders

Name : ________________________________________

Student No. (NIM) : ________________________________________

Facilitator : ________________________________________

Title : ________________________________________

________________________________________

Assessment

A. Paper structure : 7 8 9 10

B. Content : 7 8 9 10

C. Discussion : 7 8 9 10

Total point : ( A + B + C ) : 3 = _____________

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SELF ASSESSMENT

Self assessment of each lecture will be given after each lecture session, and will be marked. This mark can determine whether the student pass this block or not. Any final mark between 62 - 64 will be reconsidered with self assessment’s mark to see the student’s status. Any student with self assessment’s mark 65 or more will pass this block. And for the lower one will have to attend the remedial examination. It is important to do this self assessment cautiously, because this activity may be your ticket to pass this block just at first examination.

ASSESSMENT METHOD

Assessment in this theme consists of:

 SGD : 5%

 Final Exam : 80%

 Student Project : 15%

Final mark 65 or more considered to pass this block. Certain conditions applied for those with final mark between 62 – 64. These students will be analyzed using their self assessment’s mark. Students with final mark 62 – 64 and self assessment’s mark equal or more than 65 will also considered pass this block. The value of marking:

 A ≥ 80

 B+ >70-79

 B 65-70

GENERAL TIME TABLE FOR A AND B CLASSES

CLASS A CLASS B

TIME ACTIVITIES TIME ACTIVITIES

08.00-09.00 Lecture 09.00-10.00 Lecture

09.00-10.30 Independent learning 10.00-11.30 Student project

10.30-12.00 SGD 11.30-12.00 Break

12.00-12.30 Break 12.00-13.30 Independent learning

12.30-14.00 Student project 13.30-15.00 SGD

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TIME TABLE OF CLASSES

DAY/DATE Class A Class B ACTIVITY VENUE PIC

1 Tue Sep 26,

2017

08.00-09.00 11.00-12.00 Lecture 1 Highlight in Neuroscience

& neurological disorders Class room

dr. IA Sri Wijayanti, M.Biomed, Sp.S

09.00-10.00 12.00-13.00 Lecture 2 Anatomy of CNS & PNS Class room

Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K)

10.00-11.00 13.00-14.00 Lecture 3 Histology of CNS & PNS Class room dr. I Wayan Sugiritama, M.Kes

12.30-14.00 09.00-10.00 Independent learning

11.00-12.00 14.00-15.00 SGD Disc room Facilitator

12.00-12.30 10.00-10.30 Break

12.30-14.00 10.30-11.00 Student project

14.00-15.00 15.00-16.00 Pleanary Day 1 Class room

Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K)/ dr. I Wayan Sugiritama, M.Kes

2 Wed

27, 2017

08.00-09.00 10.00-11.00 Lecture 4 Physiology of CNS & PNS Class room dr. D.A. Inten Dwi Primayanti, M.Biomed

09.00-10.00 11.00-12.00 Lecture 5 Neuropathology of CNS &

PNS Class room

dr. Ni Putu Sri Widyani, Sp.PA

10.00-11.00 09.00-10.00 Independent learning

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14.00-15.00 15.00-16.00 Pleanary Day 2 Class room

dr. D.A. Inten Dwi Primayanti, M.Biomed / dr. Ni Putu Sri Widyani, Sp.PA

3 Thu Sep 28,

2017

08.00-09.00 10.00-11.00 Lecture 6 Clinical Pathology:

Cerebrospinal analysis Class room

Dr.dr. I Nyoman Wande, Sp.PK

09.00-10.00 11.00-12.00

Lecture 7

Pharmacology: Drugs used for seizure disorders & Parkinsonism

Class room Dr.dr. I Made Jawi, M.Kes

10.00-11.00 09.00-10.00 Independent learning

11.00-12.00 13.30-15.00 SGD Disc room Facilitator

12.00-12.30 12.00-12.30 Break

12.30-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Pleanary Day 3 Class room

Dr.dr. I Nyoman Wande, Sp.PK/ Dr.dr. I Made Jawi, M.Kes

4 Mon Oct 2,

2017

08.00-09.00 10.00-11.00 Lecture 8 Febrile Seizure Class room dr. Dewi Sutriani Mahalini, Sp.A

09.00-10.00 11.00-12.00 Lecture 9 Seizure, Epilepsy, and

Status Epilepticus Class room

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

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Pleanary Day 4 Class room

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5 Tuesday

Oct 3, 2017

08.00-09.00 10.00-11.00 Lecture 10 Dementia, Post Traumatic

Amnesia Class room

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

09.00-10.00 11.00-12.00 Lecture 11 Parkinson Disease Class room Dr.dr. DPG. PurwaSamatra, Sp.S(K)

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Pleanary Day 5 Class room

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

6 Wednesday

Oct 4, 2017

08.00-09.00 10.00-11.00 Lecture 12 Neuropathic Pain Class room Dr.dr. Thomas Eko Purwata, Sp.S(K), FAAN

09.00-10.00 11.00-12.00 Lecture 13 Migrain, Neuralgia

Trigeminal Class room

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

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

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7 Thu Oct 5,

2017

09.00-10.00 11.00-12.00 Lecture 15 Imaging: X-ray of skull

and Spine Class room

dr. Made WidhiAsih, Sp.Rad(K)

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Pleanary Day 7 Class room

Dr.dr. Made Oka Adnyana, Sp.S(K)/ dr. Made WidhiAsih, Sp.Rad(K)

8 Fri Oct 6,

2017

08.00-09.00 11.00-12.00 Lecture 16 Acute and reffered pain Class room Dr.dr. Putu Pramana, Sp.An., KMN., M.Kes

09.00-10.00 12.00-13.00 Lecture 17 Vertigo, Bell’s palsy, and

Meniere Disease Class room

dr. Ketut Widyastuti, Sp.S

10.00-11.00 13.00-14.00 Lecture 18 Neurological aspect of

Hearing Loss and Tinnitus Class room

dr. IA Sri Indrayani, Sp.S

12.30-14.00 09.00-10.00 Independent learning

11.00-12.00 14.00-15.00 SGD Disc room Facilitator

12.00-12.30 10.00-10.30 Break

12.30-14.00 10.30-11.00 Student project

14.00-15.00 15.00-16.00 Pleanary Day 8 Class room

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9 Mon Oct 9,

2017

08.00-09.00 11.00-12.00 Lecture 19 Stroke I: TIA, Cerebral

Infarction, ICB, SAH Class room

dr. IGN Budiarsa, Sp.S

09.00-10.00 12.00-13.00 Lecture 20 Stroke II: Management Class room

dr. IGN Budiarsa, Sp.S

10.00-11.00 13.00-14.00 Lecture 21 Stroke III: Surgical

Management of Stroke Class room

dr. I Wayan Niryana,M.Kes, Sp.BS(K)

12.30-14.00 09.00-10.00 Independent learning

11.00-12.00 14.00-15.00 SGD Disc room Facilitator

12.00-12.30 10.00-10.30 Break

12.30-14.00 10.30-11.00 Student project

14.00-15.00 15.00-16.00 Pleanary Day 9 Class room

dr. IGN Budiarsa, Sp.S/ dr. I Wayan Niryana, M.Kes,Sp.BS(K) 10 Tue Oct 10, 2017

08.00-09.00 10.00-11.00

Lecture 22 Complete Spinal Transaction, Acute Medullary Compression Class room Dr.dr. Tjokorda GB Mahadewa, M.Kes, Sp.BS(K)Spinal

09.00-10.00 11.00-12.00

Lecture 23

Prehospital& Initial Management of spine & spinal cord injury

Class room

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

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

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11 Wed Oct 11,

2017

08.00-09.00 10.00-11.00 Lecture 24 Neuropathy, CTS, TTS,

Peroneal Palsy Class room

dr. IA Sri Wijayanti, M.Biomed, Sp.S

09.00-10.00 11.00-12.00 Lecture 25 HNP, Radicular Syndrome

Class room dr. IA Sri Wijayanti, M.Biomed, Sp.S

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Plenary Day 11 Class room dr. IA Sri Wijayanti, M.Biomed, Sp.S

12 Thu Oct 12,

2017

08.00-09.00 10.00-11.00

Lecture 26

Coma, Encephalopathy, Hipertensive

Encephalopathy,

Class room

dr. KumaraTini, Sp.S, FINS

09.00-10.00 11.00-12.00 Lecture 27 Neurogenic Bladder Class room dr. IB. Kusuma Putra, Sp.S

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Plenary Day 12 Class room

dr. KumaraTini, Sp.S, FINS/ dr. IB. Kusuma Putra, Sp.S 13 Fri Oct 13, 2017

08.00-09.00 10.00-11.00 Lecture 28 Meningitis, Ensefalitis,

Cerebral Malaria Class room

dr. Made Susilawathi, Sp.S(K)

09.00-10.00 11.00-12.00 Lecture 29 CNS Infection HIV AIDS,

Spondylitis TB, Rabies Class room

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10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Plenary Day 13 Class room

dr. Made Susilawathi, Sp.S(K)/ dr. Putu Gede Sudira, Sp.S

14 Mon Oct 16, 2017

08.00-09.00 10.00-11.00 Lecture 30 Tetanus Neonatorum,

Tetanus, Poliomyelitis Class room

dr. Putu Witari, Sp.S

09.00-10.00 11.00-12.00 Lecture 31 Guillain Barre Syndrome,

Myasthenia Gravis Class room

dr. Komang Arimbawa, Sp.S

10.00-11.00 09.00-10.00 Independent learning

11.00-12.30 13.30-15.00 SGD Disc room Facilitator

12.30-13.00 12.00-12.30 Break

13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Plenary Day 14 Class room dr. Putu Witari, Sp.S/ dr. Komang Arimbawa, Sp.S

15

08.00-09.00 10.00-11.00

Lecture 32

Traumatic Brain Injury, Prehospital & Initial Management

Class room

Prof. Dr.dr. Sri Maliawan, Sp.BS(K)

09.00-10.00 11.00-12.00 Lecture 33 Brain Tumor and Class room

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13.00-14.00 12.30-13.30 Student project

14.00-15.00 15.00-16.00 Plenary Day 15 Class room

Prof. Dr.dr. Sri Maliawan, Sp.BS(K)/ Dr.dr. Nyoman Golden, Sp.BS(K) 16

Wed Oct 18,

2017 08.00 - Finish

08.00 -

Finish Student Project Presentation Auditorium Team

17 Thu Oct 19,

2017

08.00-10.00

10.00-12.00 Basic Clinical Skill 1: Fungsi Luhur, saraf kranialis

Skills Laboratory

dr. Putu Witari, Sp.S

18 Fri Oct 20,

2017 08.00-10.00 10.00-12.00

Basic Clinical Skill 2: Sistem Motorik,

Koordinasi dan sensorik

Skills Laboratory

dr. IA Sri Wijayanti, M.Biomed, Sp.S 19 Mon Oct 23, 2017

08.00-10.00 10.00-12.00

Basic Clinical Skill 3:

- Refleks fisiologis, patologis dan primitif - Pemeriksaan tulang

belakang

- Tanda perangsangan meningeal dan tanda ischialgia

Skills Laboratory

dr. Putu Gede Sudira, Sp.S

20 Tue Oct 24,

2017

08.00-10.00 10.00-12.00

Basic Clinical Skill 4: Pemeriksaan Diagnostik Radiologi (CT-skenotak dan interpretasinya), Punksi Lumbal dan elektrodiagnostik lainnya

Skills Laboratory

dr. IA Sri Indrayani, Sp.S

21 Wed Oct 25,

2017 Pre- Evaluation Break

22 Thu Oct 26,

2017 Examination

Class Room : R. 4.02 (4th Floor)

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LEARNING PROGRAMS LECTURE 1

HIGHLIGHT NEUROSCIENCE AND NEUROLOGICAL DISORDERS

dr. Ida Ayu Sri Wijayanti, M.Biomed, Sp.S*

*Neurology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

Basic structure

The nervous system consists of the brain, spinal cord and peripheral nerves. It is made up of nerve cells, called neurons, and supporting cells called glial cells.

There are three main kinds of neurons. Sensory neurons are coupled to receptors specialised to detect andrespond to different attributes of the internal and externalenvironment. The receptors sensitive to changes in light, sound, mechanical and chemical stimuli subserve the sensory modalities of vision, hearing, touch, smell and taste.When mechanical, thermal or chemical stimuli to the skin exceed a certain intensity, they can cause tissue damage and a special set of receptors called nociceptors are activated; these give rise both to protective reflexes and tothe sensation of pain.

Motor neurons, which control the activity of muscles, are responsible for all forms of behaviour including speech. Interposed between sensory and motor neurons are Interneurones. These are by far the most numerous (in the human brain). Interneurons mediate simple reflexes as well as being responsible for the highest functions of the brain. Glial cells, long thought to have a purely supporting function to the neurons, are now known to make an important contribution to the development of the nervous system and to its function in the adult brain. While much more numerous, they do not transmit information in the way that neurons do.

Neurons have an architecture that consists of a cell body and two sets of additional compartments called ‘processes’. One of these sets are called axons; their job is to transmit information from the neuron on to others to which it is connected. The other set are called dendrites - their job is to receive the information being transmitted by the axons of other neurons. Both of these processes participate in the specialised contacts called synapses. Neurons are organised into complex chainsand networks that are the pathways through which information in the nervous system is transmitted.

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control of vital functions such as breathing and blood pressure. Within these are networks of neurons whose activity controls these functions. Arising from the roof of the hind-brain is the cerebellum, which plays an absolutely central role in thecontrol and timing of movements.

The midbrain contains groups of neurons, each of which seem to use predominantly a particular type of chemical messenger, but all of which project up to cerebral hemispheres. It is thought that these can modulate the activity of neurons in the higher centres of the brain to mediate such functions as sleep, attention or reward. The diencephalon is divided into two very different areas called the thalamus and the hypothalamus: The thalamus relays impulses from all sensory systems to the cerebral cortex, which in turn sends messages back to the thalamus. This back-and-forward aspect of connectivity in the brain is intriguing - information doesn’t just travel one way. The hypothalamus controls functions such as eating and drinking, and it also regulates the release of hormones involved in sexual functions.

The cerebral hemispheres consist of a core, the basal ganglia, and an extensive but thin surrounding sheet of neurons making up the grey matter of the cerebral cortex. The basal ganglia play a central role in the initiation and control of movement. Packed into the limited space of the skull, the cerebral cortex is thrown into folds that weave in and out to enable a much larger surface area for the sheet of neurons than would otherwise be possible. This cortical tissue is the most highly developed area of the brain in humans. It is divided into a large number of discrete areas, each distinguishable in terms of its layers and connections. The functions of many of these areas are known - such as the visual, auditory, and olfactory areas, the sensory areas receiving from the skin (called the somaesthetic areas) and various motor areas. The pathways from the sensory receptors to the cortex and from cortex to the muscles cross over from one side to the other. Thus movements of the right side of the body are controlled by the left side of the cortex. Similarly, the left half of the body sends sensory signals to the right hemisphere such that, for example, sounds in the left ear mainly reach the right cortex. However, the two halves of the brain do not work in isolation - for the left and right cerebral cortex are connected by a large fibre tract called the corpus callosum.

The cerebral cortex is required for voluntary actions, language, speech and higher functions such as thinking and remembering. Many of these functions are carried out by both sides of the brain, but some are largely lateralised to one cerebral hemisphere or the other. Areas concerned with some of these higher functions, such as speech (which is lateralised in the left hemisphere in most people), have been identified. However there is much still to be learned, particularly about such fascinating issues as consciousness, and so the study of the functions of the cerebral cortex is one of the most exciting and active areas of research in Neuroscience.

Fundamental of Neurological Disorders

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The type of neurological disturbance from which a patient is suffering can usually be determined from a carefully obtained clinical history even before the physical examination or any further tests are performed. In many patients, the history alone permits the assignment of a precise diagnosis, but only if the physician has been listening closely to the patient. Skillful history taking is the distinguishing mark of a good clinician.

In any branch of clinical medicine, not just in neurology, a good history can be obtained only if the patient has confidence in the physician. Introduce yourself to the patient and take the history in a place offering the necessary privacy and discretion. The patient should be comfortably seated and emotionally at ease, as far as the circumstances allow, and must not feel rushed. If someone else is present during the interview, e. g., a medical student, introduce this person and make sure the patient really has no objection to his or her presence. Persons other than the physician taking the history should behave discreetly and keep themselves somewhat in the background. The history should be detailed and complete and should be taken by, or under the supervision of, an experienced clinician, as far as possible. While interviewing the patient, observe these principles: in the beginning the patient should be doing most of the talking and you should say as little as possible.

Every patient has the right to be treated courteously and tactfully and to receive the physician’s full attention during an appropriately set period. You should perform a meticulous physical examination only after you have listened carefully to the patient’s story and filled it out with further, detailed questioning. The patient has the right to a full explanation of your findings and of what they imply about his or her illness. You should explain these matters truthfully, in language that the patient can understand and with due respect for his or her feelings. You will often find yourself having to steer a difficult course between bluntness and euphemism.

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LECTURE 2

ANATOMY OF NERVUS SYSTEM

Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K)* *Anatomy Department, School of Medicine, Faculty of Medicine, Universitas Udayana

The needs of living things for feeding, feeling safe, comfortable and finding a partner to breed need information from outside or from within the body to be able to respond in an integral way. The creature required cells that have specialization easy to receive and convey stimulus. These cells are called nerve cells. In the body thenerve cells are arranged in the Central Nervous System (CNS), Peripheral Nervous Syatem (PNS) and Autonomic Nervous System (ANS). By its nature nerve cells are divided into motor and sensory nerves. Neuro anatomy studies the nervous system, its organization and its functions.

The CNS is tubular shaped with a swollen cranial part, consisting of the brain, brainstem and spinal cord. The CNS consists of many nuclei and nerve fibers arranged in tract. That brings the sensory stimuli of the spinal cord to the higher centers called tractus ascendens carrying sensory impulses. The down fibers from the brain to the spinal cord is called tractus descendentes carrying motor sensoric.

The PNS is nerve fibers that comes out of the CNS and serves all the organs of the body, both motor and sensory. The CNS consists of 12 pairs cranial nerves (nervi craniales) coming out from the brain stem and consist of 31-32 pairs peripheral nerves.

The ANS is motoric in nature serving smooth muscle existing in the internal organs (visceral organs), glandular muscles and also serve the heart muscle.

Neural cells at both the center and the periphery are maintained by glial cells In its function nerve cells need the help of other nerve cells to convey messages either to the center or to the periphery. The relationship between nerves is called a synapse. Communication in synapses is done through a chemical substance called neurotransmitter.

Learning Task.

1. Draw a chart of a nerve cell, its parts and its types!

2. Explain what are synapses, neurotransmitters and types of synaptic anatomical relationships!

3. Explain the properties of the nerves according to the impulse it carries! 4. Describe all parts of the CNS as well as its function!

5. Explain the anatomy of PNS, the amount and its nature! 6. Name all cranial nerves and their properties!

7. Explain about SSO and its properties!

8. What is the difference between sympathetic and parasympathetic nerves?

9. Distinguish the tract and nerve fibers. Between nuclei and ganglion. Between afferent and afferent fibers!

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Case 1

A young man complained every sport his lips always dry. Conversely if sleep like runny. 1. What autonomous nerve is active in active motion / exercise and during sleep?

2. Describe the location of the sympathetic nerve center, the organ served, and its effects! 3. Explain the location of the parasympathetic center, the organ served and its effects!

Case 2.

A housewife suffers a spinal fracture from trauma. The mother experiences muscle paralysis as well as loss of skin sensation from below the navel down. There is hyperreflesi in the knee joint. Doctors suspect damage has occurred on Upper Motor Neuron due to spinal cord injury.

1. Draw the cross-sectional chart of the spinal cord, its parts and its functions!

2. Explain what is meant by Upper Motor Neuron and Lower Motor Neuron! Differences between tractus ascendentes and descendentes!

Case 3.

When a new wake up a father can not move half his body, his lips can not close tight and one eyelid can not be blinked and unclear voice. Suspected the father suffered a stroke involving the cranial nerve.

1. Name the cranial nerves, the structure served and their nature!

Case 4.

When your bare feet step on a lit cigarette butt, you pull your legs very fast. The reflex movements we have are useful to protect our bodies from danger.

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LECTURE 3

HISTOLOGY OF NERVUS SYSTEM

Dr. Wayan Sugiritama, M.Kes*

*Histology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

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.

Trigger Case 1:

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Learning Tasks:

1. Differentiate the histological structure of the cerebellum with the cerebrum! 2. Describe the structure of connective tissue that covered the brain!

3. Why subdural space considered as “potential space” and what are it’s clinical importance? 4. Decreased of motoric and sensory function on patient’s leg may caused by spinal cord

injury, please explain its structure!

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

6. Explain the regeneration of the brain and nerve after the injury!

Trigger Case 2:

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

Learning Tasks:

1. Explain the structure of plexus choroideus which is produce the CSF! 2. Explain the production and absorption of CSF (cerebrospinal fluid)!

3. Explain the role of the blood-CSF barrier in maintained the chemical stability of the CSF! 4. Describe the structure of neuroglial cell which is have a role in circulation of CSF!

Trigger Case 3

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

Learning Tasks:

1. Explain the structure of high selective barrier between blood borne substances and neural tissue of CNS!

2. How this barrier can protect the neural tissue of CNS from dangerous substances (e.g. microorganism) on the blood, explain your answer!

3. What is the clinical importance this barrier in treatment of disease in CNS, explain your answer!

Self Assessment

1. Explain the general structure of neuron!

2. Mention and explain classification of neuron according to their structure and their function!

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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!

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LECTURE 4

PHYSIOLOGY OF NERVUS SYSTEM

dr. I Dewa Ayu Inten Dwi Primayanti, M.Biomed*

*Physiology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

The nervous system is unique in the vast complexity of thought processes and control actions it can perform. It receives each minute literally millions of bits of information from the different sensory nerves and sensory organs and then integrates all these to determine responses to be made by the body.

The nervous system consist of a highly complex aggregation of cells, part of which is a communication network and another part a supportive matrix. The communication network is formed by neurons, which are the functional cellular units of nervous system. The nervous system includes both sensory (input) and motor (output) system interconnected by complex integrative mechanisms. The nervous system divided into the Central Nervous System (CNS) and the Peripheral Nervous System. The central nervous system includes the brain and spinal cord. The peripheral nervous system has afferent ( sensory) neurons that bring infoemation into the Central Nervous System , and efferent neurons that carry information away from the CNS back to various parts of the body. The efferent neurons include somatic motor neurons, which control skeletal muscles, and autonomic neurons, which control smooth and cardiac muscle, gland and some adipose tissue. Autonomic neurons are subdivided into sympathetic and parasympathetic branches.

Neurons have a cell body with a nucleus and organelles to direct cellular activity, dendrites to receives incoming signals and an axon to transmit electrical signal from the ceel body to the axon terminal.

The nervous system is composed primarily of two cell types are found in central nervous system & peripheral nervous system. The neuron is the basic structural and functional unit of the Nervous System 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.

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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.

Much of the activity in the Nervous system 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

LEARNING TASK

1. Describe functional type of neurons : afferent, autonomic, brain, central, efferent, enteric, parasympathetic, peripheral, sensory, somatic motor, spinal, sympathetic!

2. Explained about:

a. Polarization, depolarization, repolarization and hyperpolarization.

b. Action potential, grade potential ( Explain how the graded potential and action potential differ !)

c. Resting membrane potential.

d. Ion channels ( List four major type of ion channels, are they chemically-gated, mechanically-gated or voltage-gated?)

3. Define three ways neurotransmitters are removed from the synapse, explained it!

4. What is the function of the mitokondria in a cell and how do mitokondria get to the axon terminal?

5. The nervous system secretes neurocrines. Mention its and the receptor location! 6. What do you know about:

a. EPSP ( excitatory postsynaptic potential) and IPSP ( Inhibitory postsynaptic potential)?

b. Fast synaptic potential & slow synaptic potential?

7. A man falls into deep sleep with one arm under his head. This arm is paralyzed when he awakens, but it tingles, and pain sensation in it is still intact. What is the reason for the loss of the motor function without loss of pain sensation is that in the nerves to his arm?

8. What is the primary function of myelin, microglia, ependymal cells? 9. Please explain the function of the brain based on the region!

10. Awoman was walking in the park. She saw a very beautiful flower. She was very happy and picked the flower. Explain the neuro-physiological processes that occur in that woman!

SELF ASSESSMENT

1. Describe the structure of neuron and explain significance of its principal regions! 2. Classify neurons on the basis of their structure and function!

3. Describe the location, the major types, and functions of the supporting cells! 4. Explain how the graded potential and action potential differ!

5. Define polarization, depolarization, repolarization and hyperpolarization!

6. Explain the actions of voltage regulated Na+ and K+ channels and describe the event that occur during the production of an action potential!

7. Explain how action potentials are regenerated a long myelinated and non myelinated axon!

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9. Compare the characteristics of EPSPs and action potential! 10. Explain the synaptic transmission exhibits special characteristic!

11. Explain how sensory receptors are categorizeds. Give examples of functional of functional categories and explain how tonic and phasic receptors differ!

12. Describe the classification of the sensory division – sensory receptors!

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

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

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

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LECTURE 5

NEUROPATHOLOGY OF NERVUS SYSTEM

Dr. dr. Ni Putu Sriwidyani, Sp.PA*

*Pathology of Anatomy Department, School of Medicine, Faculty of Medicine, Universitas Udayana

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. In central nervous system pathology will discussed about cerebral edema, hydrocephalus, and raised intracranial pressure and herniation, and some common central nervous system diseases.

The two components of peripheral nerves are axons and myelin sheaths made by Schwann cells. Injuries to either of these components may result in a peripheral neuropathy. In peripheral nerve diseases will discussed about general type of peripheral nerve injury, anatomic patterns of peripheral neuropathies and some specific peripheral neuropathies.

Case 1

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

Question:

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

Case 2

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

Case 3

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SELF ASSESMENT

Describe and give some example of:

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

3. Trauma affecting CNS. 4. Cerebrovascular disease. 5. CNS Infection.

6. Demyelinating disease. 7. Degenerative disease of CNS. 8. Tumors of CNS.

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LECTURE 6

CEREBROSPINAL FLUID ANALYSIS Dr. dr. I Nyoman Wande, Sp.PK*

*Clinical Pathology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

Abstract

The cerebrospinal fluid (CSF) is a dynamic, metabolically active substance that has many important functions. It is invaluable as a diagnostic aid in the evaluation of inflammatory conditions, infectious or non infectious, involving the brain, spinal cord, and meninges. CSF is obtained with relative ease by lumbar puncture (LP). Alterations in CSF constituents may be similar in different pathologic processes and cause difficulties in interpretation. Combining a set of CSF variables referred to as routine parameters (i.e. determination of protein, albumin, immunoglobulin, glucose, lactate, and cellular changes, as well as specific antigen and antibody testing for infectious agents) will increase the diagnostic sensitivity and specificity.

CSF should be analysed immediately after collection. If storage is needed 12 ml of CSF should be partitioned into three to four sterile tubes. Albumin CSF/serum ratio (Qalb) should be preferred to total protein measurement and normal upper limits should be related to patients’ age. Elevated Qalb is a non-specific finding but occurs mainly in bacterial, cryptococcal, and tuberculous meningitis, leptomingeal metastases as well as acute and chronic demyelinating polyneuropathies. Pathological decrease of the CSF/serum glucose ratio or an increase in lactate concentration indicates bacterial or fungal meningitis or leptomeningeal metastases. Intrathecal immunoglobulin G synthesis is best demonstrated by isoelectric focusing followed by specific staining. Cellular morphology (cytological staining) should be evaluated whenever pleocytosis is found or leptomeningeal metastases or pathological bleeding is suspected. Computed tomography-negative intrathecal bleeding should be investigated by bilirubin detection.

Learning Objective

1. Describe the formation and location of cerebrospinal fluid (CSF)! 2. Describe the appearance and state the composition of normal CSF!

3. Understand the clinical significance of performing a spinal tap and accurately evaluating CSF!

4. Discuss the importance and significance of utilizing the properly collected CSF specimen for chemistry, hematology, microbiology and immumologic testing!

5. Know how to examine and report the appearance of CSF.

6. Be able to perform a manual white blood cell chamber count on a CSF specimen.

7. Be able to correctly calculate the white blood cell count for CSF specimens when given the results of a chamber count performed using various dilutions.

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Scenario 1:

A man, 30 years old, came to the emergency room with complain about unconscious. Previously the patient had a bloody cough for 3 months, night fever and body weight decreased since 4 months ago. On physical examination was found: unconscious patient, blood pressure 130/80 mmHg, pulse rate: 100 times/ minute, respiration rate: 40 times/ minute, axillary temperature 37,90C. Patients planned to do cerebrospinal fluids analysis.

Learning task:

1. What is a lumbar puncture (spinal tap) and how is it performed?

2. Which of the following is an abnormal cerebrospinal fluid (CSF) finding? 3. Which of the following CSF results suggests fungal meningitis?

4. Which of the following is true about the CSF changes in patients with tuberculous meningitis?

5. Which of the following is most likely to cause a low CSF glucose?

Scenario 2:

A man, 25 years old, came to the emergency room with complain about Seizures. Previously the patient had a cephalgia for 3 months, impaired vision since 1 months ago. On physical examination was found: conscious patient, blood pressure 120/80 mmHg, pulse rate: 80 times/minute, respiration rate: 25 times/minute, axillary temperature 36,50C. Patients planned

to do cerebrospinal fluids analysis.

1. Are there other reasons to do a lumbar puncture?

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LECTURE 7

PHARMACOLOGY: DRUGS USED FOR SEIZURE DISORDERS & PARKINSONISM & OTHER MOVEMENT DISORDERS

Dr. dr. I Made Jawi, M.Kes*

*Pharmacology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

AIMS

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

LEARNING OUTCOMES

Apply concepts and principles of drugs used for seizure.

CURRICULUM CONTENT

1. Basic pharmacology of anti seizure drugs

- Drugs used in partial seizures & generalized tonic-clonic seizures.

- Drugs used in generalized seizures.

- Other drugs used in management of epilepsy. 2. Clinical pharmacology of anti seizure drugs

- Management of epilepsy.

- Special aspect of the toxicology of anti seizure drugs.

ABSTRACT

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

SCENARIO

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LEARNING TASK

1. Describe how you as a doctor would address this situation! 2. Describe anti seizure drugs using in seizure patients!

3. Describe adverse effect of anti seizure drugs using in seizure patients!

SELF ASSESMENT

1. What is the definition of fetal hydantoin syndrome!

2. Which one of antiseizure drugs can cause gingival hyperplasia!

3. Can you describe the interaction of antiseizure drugs with the other drugs! 4. What is the treatment of patient with status epilepticus!

AIMS

1. Describe the rationale drugs used to treat parkinson’s disease. 2. Describe the desired theraupetic outcomes for parkinson’s disease. 3. Develop a education plan for people diagnosed with parkinson’s disease.

LEARNING OUTCOMES

Apply concepts and principles of drugs used for parkinson’s disease.

CURRICULUM CONTENT

Drug therapy for Parkinson’s Disease

- Drug class: Dopamine Agonists

- Drug class: COMT Inhibitor

- Drug class: Anti cholinergic Agents

- Drug class: Miscellaneous Anti parkinsonism Agents

ABSTRACT

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SCENARIO

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

LEARNING TASK

1. What symptoms can be expected to improve?

2. What problems could also arise from starting this medication?

3. Discuss the normal course of progsession of Parkinson’s disease and include the rationale for drug therapy to alleviate the symptoms!

4. List drugs which will give to the patient who has parkinsonism!

5. Explain why do you choose L-dopa and not dopamine to treat Parkinson’s disease! 6. Explain why levo-dopa could not be combined with pyridoxine!

7. Describe the benefit combination of levodopa with carbidopa in the treatment of Parkinsonism!

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

SELF ASSESMENT

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LECTURE 8

FEBRILE SEIZURE IN CHILDREN

dr. Dewi Sutriani Mahalini, Sp.A*

*Paediatry Department, School of Medicine, Faculty of Medicine, Universitas Udayana

Aims:

Describes concepts, definition, pathophysiology, classification, diagnosis and management of febrile seizures in children.

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 of febrile seizure and long term management for prevention recurrent seizure!

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

Curriculum contents:

1. Definition, etiology and pathophysiology of febrile seizure in children. 2. Classification of febrile seizure,

3. Recommendation for management febrile seizure in children.

4. Recommendation for immediate medical management of acute seizure and status epilepticus.

5. Risk factors of recurrent febrile seizures and genetic epilepsy with febrile seizures plus (GEFS+).

6. Long term management for prevention of recurrent febrile seizure (intermittent and long term prophylaxis).

Abstract

Febrile seizures (FS) are the most common seizure disorder in childhood. Seizures with fever occur in 3- 5% of children in North America and Europe, and in up to 14% of children in Asia. It affects both boys and girls equally, mainly between 6 and 36 months with a peak at an age of 18 months.

A febrile seizure (FS) is a disorder that presents between 6 months and 5 years of age with convulsions and fever (temperatures above 38oC) but without evidence of intracranial

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in 24 hours. Complex febrile seizure also associated with post-ictal neurologic abnormalities, more frequently a post ictal palsy (Todd’s palsy) or with previous neurologic deficits.

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, neuronal abnormality and prolonged stay in a neonatal unit.

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 there is a history of febrile seizure or epilepsy in the family, the age is younger than 12 months when first febrile seizure occurred, temperature less than 39oC when seizures, the short time interval

between the onset of fever and seizures.

The etiology of FS is multifactorial; an autosomal dominant inheritance with reduced penetrance has been described in several families. Several chromosomal loci have been identified, particularly those on 19q and chromosome 2. 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 history taking and physical examination. The initial evaluation is intended to exclusion of intracranial process or metabolic disorder. Immediate medical management includes treatment of the seizure if still continuing. Benzodiazepines administered rectally, buccally or nasally are useful for rapid control. 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. Long term treatment with sodium valproate may be beneficial in children with very frequent atypical febrile seizures, particularly those with recurrent prolonged seizures, duration of seizures more than 15 minutes, focal seizures, or in children with neurological disorders before or after seizures (such as cerebral palsi, hydrocephalus, hemiparesis).

Case 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 duration 5 minutes, the type of seizure were generalized tonic, with both eyes looking upward. A few minutes after seizure finished, she cried loudly. The physical examination revealed: alert, respiration 28 times/minutes, pulse 100 times/minutes, temperature 39.5oC. The urination was clear and yellow, but the patient had

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Case 2

A 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. Type of seizure were generalized tonic clonic, both eyes looking upward. She look weak after seizure and still unconscious. The past history were patient already had seizure 3 times episode since 12 months of age.

History of delivery were spontaneous, birth body weight 2000 grams and severe asphyxia. The physical examination revealed: respiration rate 30 times/minutes, pulse 120 times/minutes, rectal temperature 40.0oC. She also had history of cough and difficult breathing since 3 days

before admission. The urination was clear and yellow, defecation was normal.

Case 3

A boy, 3 years of age, came to the emergency unit with main complaint serial seizure. The first seizure occur 5 hours before admission, he looks weak after seizure and crying loudly 10 minutes later. Second seizure occur since 20 minutes ago and the seizure still continued until the patient arrive at emergency unit. Patient had been treated with diazepam rectally twice prehospital, but the seizure still continued. Type of seizure were tonic clonic and just affect the right limbs. He look weak after seizure and still unconscious. The past history: patient already had seizure, 2 times episodes since 8 months of age, history of delivery were sectio cesarea from mother with severe preeclampsia, the baby was preterm and had severe asphyxia. The physical examination revealed, respiration 54 times/minutes, pulse 120 times/minutes, rectal temperature 39,5oC. The neurological examination revealed bad posture with limbs spasticity. He had been

diagnosed with Cerebral palsy & failure to thrive. He also had history of cough and difficult breathing since 1 days before admission. The urination was clear and yellow, defecation normal.

Learning task

Answer the questions below for all three cases above!

1. 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?

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Self assessment

1. Describe definition of febrile seizure in children!

2. Describe classification of febrile seizure in children and its differentiation! 3. Describe etiology and patophysiology of febrile seizure in children! 4. Describe the management of acute seizure in emergency unit!

5. Describe the long term management for prevention recurrent seizure! 6. Describe prognosis of febrile seizure and risk factors that influences its!

References

1. Ismael S, Pusponegoro HD, Widodo DP, Mangunatmadja I, Handryastuti S, Editor. Rekomendasi penatalaksanaan kejang demam. UKK Neurologi IDAI, 2016.

2. Ismael S, Pusponegoro HD, Widodo DP, Mangunatmadja I, Handryastuti S, Editor. Rekomendasi penatalaksanaan status epilepticus. UKK Neurologi IDAI, 2016.

3. American Academy of Pediatrics. Febrile Seizures: guideline for the neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics 2011;127: 389

4. Hampers LC, Spina LA.Evaluation and management of pediatric febrile seizures in the emergency department. Med Clin N Am 2011; 29:83–93.

5. Kasperaviciute D, Catarino CB, Matarin M, Leu C, Novy J, Tostevin A, et al. Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A. Brain 2013; 136: 3140–50

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LECTURE 9

SEIZURE, EPILEPSY AND STATUS EPILEPTICUS

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

*Neurology Department, School of Medicine, Faculty of Medicine, Universitas Udayana

Aims:

Describe the pathophysiology, diagnosis, early manage and referral patient with seizures.

Learning Outcome:

1. Describe the role of neurotransmitters on patophysiology of seizures! 2. Describe the neurological sign and symptom of seizures!

3. Describe the classification of epilepsy!

4. Describe the Electroencephalography in diagnose of epilepsy!

5. Describe early

Gambar

Table 1. Comparison of Vascular Dementia and Alzheimer’s dementia.

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