SEMESTER V BLOCK 9v1.fk.ub.ac.id/id/pu/BlockIX TA 2009-2010 Student...5) Sudjari, dr. (Department of Parasitology) 6) Mudjiwiyono, dr, SpPA. (Department of Pathology Anatomy) 7) Dr

SEMESTER V

BLOCK 9

The Nervous System, Psychiatry,

Eye, Ear, Nose and Throat

BRAWIJAYA UNIVERSITY FACULTY OF MEDICINE

MALANG 2009

CONTENT

1. Block Name

2. Period of Teaching‐ Learning / Study Load

3. Block Team

4. Block Introduction

5. MODUL

6. Relation to Other Blocks

7. Block Schedule

8. References

9. Block Assessment

SEMESTER V BLOCK 9

The Nervous System, Psychiatry, Eye, Ear, Nose and Throat

1. Block Name

A. The Nervous System, Psychiatry, Eye, Ear, Nose, and Throat

2. Period of Teaching‐ Learning / Study Load

A. Semester V / Block 9 , 14 sks

3. Block Team :

A. Block Coordinator

1) dr. Shahdevi Nandar, SpS

B. Block Secretary

1) dr. Nadia Artha Dewi, SpM

C. Core Contributors

1) Shadevi Nandar, dr, SpS. (Department of Neurology)

2) Masruroh Rahayu, dr, MKes. (Department of Neurology)

3) Happy I. H, dr, SpKJ. (Department of Psychiatry)

4) Sri Fuad Hidajati, dr, SpKJ. (Department of Psychiatry)

5) Seskoati, dr, SpM. (Department of Opthalmology)

6) J. Bambang Soemantri, dr, SpTHT‐KL(K). (Department of Ear, Nose, and Throat)

D. Supporting Contributors

1) Andi Ansharullah, dr, DAAK. (Department of Anatomy)

2) Dr. Retty Ratnawati, dr, MKes. (Department of Physiology)

3) Hidayat Suyuti, dr, PhD, SpM. (Department of Biochemistry)

4) Dr. Nurdiana, dr, MKes. (Department of Pharmacology)

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5) Sudjari, dr. (Department of Parasitology)

6) Mudjiwiyono, dr, SpPA. (Department of Pathology Anatomy)

7) Dr. Sri Winarsih, dra, Apt, MSI. (Department of Microbilogy)

8) Tita Hariyanti, dr, MMRS. (Department of Public Health)

9) Masdar Muid, dr, SpA. (Department of Pediatrics)

10) Ari Prasetya, dr, SpEM. (Department of Emergency Medicine)

11) Indraswati, dr, SpRad. (Department of Radiology)

12) Moch Ridwan, dr, SpRM. (Department of Medical Rehabilitation)

13) Agus Choirul Anab, dr, SpB. (Department of Neurosurgery)

14) Isngadi, dr, SpAn. (Department of Anaesthesiology)

15) Lintang K, dr, SpA. (Department of Pediatrics)

E. Attending Departments

1) Neurology

2) Psychiatry

3) Eye

4) Ear, Nose, and Throat

5) Anaesthesiology

6) Anatomy‐Histology

7) Biochemistry

8) Emergency Medicine

9) Forensic Medicine

10) Medical Rehabilitation

11) Microbiology

12) Neurosurgery

13) Parasitology

14) Pathology Anatpmy

15) Pediatric

16) Pharmacology

17) Physiology

18) Public health

19) Radiology

F. Attending Facilitators

1) Dr. Nurdiana, dr, MKes.

2) Dr. med. Tommy A. Nazwar, dr.

3) Agus Choirul Anab, dr, SpBS.

4) Andi Ansharullah, dr, DAAK.

5) Ari Prasetya, dr, SpEM.

6) Arliek Rio Yulia, dr, MKes.

7) Bambang Sumantri, dr, MKes.

8) Bambang Sumantri, dr, SpTHT.

9) Daniek Agustin, dr, MS.

10) Dian Nugrahenny, dr.

11) Habibah Aurora, dr.

12) Hidayat Suyuti, dr, PhD, SpM.

13) Masruroh Rahayu, dr, MKes.

14) Moch.Ridwan, dr, SpRM.

15) Mudjiwiyono, dr, SpPA.

16) Shahdevi Nandar, dr, SpS.

17) Sudjari, dr, MKes.

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4. Block Introduction

A. Block Overview

1) Nervous system will be held on fifth semester within 13 weeks, 24 August until 4

December 2009. In this block students will learn about sub system disease of

neurology, psychiatry, ophthalmology and ENT. This block will use problem base

learning strategy with discussion, tutorial and skill station method.

B. Learning Outcomes (Expecting Competencies)

1) Capable and understand the diseases of neurology field.

2) Capable and understand the diseases of ophthalmology field.

3) Capable and understand the diseases of psychiatric field.

4) Capable and understand the diseases of ear, nose and throat field.

C. Learning Objectives

1) Capable and demonstrate management of the Nervous System, Psychiatric, Eye, and

ENT.

2) Capable and demonstrate communication skills of the Nervous System, Psychiatric,

Eye, and ENT.

3) Capable and demonstrate specific physical examination on the Nervous System,

Psychiatric, Eye, and ENT.

D. Teaching Learning Activities

1) Non Modul Lecturing

2) Departmental Work Practice

3) Modulated Small Group Tutorials

4) Skill Training in Skill Laboratory

5) Task

E. Block Contents

1) Non Modul Departmental Topics related to the Block Theme (see below)

2) Practical Departmental Works (If Any)

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3) Modul (see below)

4) Skill related to the Modul / Block Theme

a) Communication and History Taking on Nerve System, Psychiatric, Eye, and ENT.

b) Procedural Skills on Nervous System, Psychiatric, Eye, and ENT.

c) Procedural Skills on medical rehabilitation.

d) Procedural Skills on emergency medicine.

e) Rational drug therapy of pharmacology.

F. Skill Station

1) Neurology

2) Psychiatric

3) Ophthalmology

4) ENT

5) Emergency Medicine

6) Medical Rehabilitation

7) Pharmacology

5. MODUL

A. Modul :

1) Modul 1 : Stroke

2) Modul 2 : Meningitis

3) Modul 3 : Schizophrenia

4) Modul 4 : Cataract

5) Modul 5 : Hearing Loss

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B. Learning Objective Mapping

Mark one or more “ √ “ in the appropriate Learning Objective of each modul :

Learning Objective Modul

1 2 3 4 5

1 Able to present anamnesis to gather optimal and useful information

2 Able to elaborate and analyze the information from patient

3 Able to professionally facilitate patient emotional words

4 Able to professionally respond to verbal or non verbal patient’s attitude

5 Able to conduct appropriate physical examination

6 Able to establish appropriate diagnosis

7 Able to recommend other appropriate supporting examination needed to establish diagnosis

8 Able to perform Medical Record from all patient’s medical datas and findings

9 Able to design appropriate treatment management plan

10 Able to refer and consult the patient to the more competent doctor related to the patient’s disease

11 Able to advice and offer the patient to promote his health in the future

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C. Topic and Topic Tree

6. Relation to Other Blocks

The student shoud refer to following Blocks :

A. General Structure and Function of The nervous System, Eye, ENT

B. Principles of Molecular / Cellular Biology

C. Effective Communication Skill

D. General History Taking

E. General Survey and Vital Signs

F. Sign and Symptoms of PAIN

7. Block Schedule

8. References

References both for modul and non modul are listed listed as below

See below and every laboratory.

STROKE HEARING LOSS CATARACT MENINGITIS SCHIZOPHRENIA

Non Modul Lectures on The Nervous

Pathologic Changes of The Nervous System, Psychiatric, Eye, and ENT

Related Clinical Sciences needed in Diagnosing,Treating, and Rehabilitating Diseases and Disables in Neurology,

Psychiatric, Eye, and ENT

Basic Structure and Function of The Nervous System,

Psychiatric, Eye, and ENT

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9. Block Assessment

A. Non Modul Assessment

1) Midsemester I Written Examination

2) Midsemester II Written Examination

3) End Semester Remedial Examination

4) Work Practice Examination (If Any)

Final Score after weighting (according to Department’s internal regulation of

assessment) shoud be recorded in term MKDI (Matakuliah Disiplin Ilmu) ‘s Score of each

Discipline involved in this Block

B. Modul Assessment

1) Learning Skill Process Evaluation through the Tutorial using Obervation Sheet

prepared by Jurusan.

2) Modul Examination at the end of T‐L Process. End Semester Remedial Modul

Examination

Final Score after weighting (according to The Jurusan Assessment Regulation) shoud be

recorded in term of MKK (Matakuliah kompetensi)’s Score. And should be converted into

Grade.

C. Skill Assessmen

D. Objective Structured Clinical Examination

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TIME SCHEDULE Ac.Year 2009/2010 The Nervous System, Psychiatry, Eye, Ear, Nose and Throat

WEEK 1 WEEK 2

TIME Monday Tuesday Wednesday Thursday Friday Monday Tuesday Wednesday Thursday Friday 24-8-2009 25-8-2009 26-8-2009 27-8-2009 28-8-2009 31-8-2009 1-9-2009 2-9-2009 3-9-2009 4-9-2009

07.00 – 08.00

NON –SYSTEM SUBJECT


08.00 – 09.00

OVERVIEW

Basic Neurology

Neuro- physiology 1

Epilepsy 1 Neuro- Anatomy 4

Neuro- physiology 5

Microbiology Neuro 1

Lecture Meningitis 1

09.00 – 10.00

Neuro- Anatomy 1

Topical Diagnosis

Neuro- physiology 2

Epilepsy 2 Neuro- Anatomy 5

Neuro- physiology 6

Microbiology Neuro 2

Lecture Meningitis 2

10.00 – 11.00

Neuro- Anatomy 2

Neuro- physiology 3

Entomology 1

Neuro- Anatomy 6

Neuro- physiology 7

Parasitology Neuro 1

Entomology 3

11.00 – 12.00 Neuro- Anatomy 3

Neuro- Physiology 4

Entomology 2

Neuro- physiology 8

Parasitology Neuro 2

Entomology 4

12.00 – 13.00 LUNCH BREAK LUNCH BREAK 13.00 – 14.00 Practice

Neuro- Anatomy

History Taking Neurology

NON –

SISTEM SUBJECT

Practice Neuro- Anatomy

Discussion Module Meningitis

Skill GCS & Meningeal Sign

NON –

SISTEM SUBJECT

14.00 – 15.00 15.00 – 15.30

Notes :

Green colour : Lecture; Purple : Discussion / Skill; Blue : Lunch break; Yellow: Self study; White: Non-System subject Lecture : 3 classes (Class A: R.K.I ; Class B: R.6.04; English class: R.4.08) Discussion & Skill : 12 small classes (R.K.I, R.6.04, R.4.08, R.2.01 – R.2.07, R.3.10 - R.3.11) Laboratory involved : Neurology : 33 h Anatomy Histology : 10 h Parasitology : 2 h Biochemic Eye : 1 h

Psychiatric : 16 h Patology Anatomy : 4 h Public Health : 2 h Pediatric : 5 h Eye : 28 h Pharmacology : 10 h Microbiology : 6 h Anaesthesi : 2 h ENT : 23 h Neurosurgery : 9 h Forensic : 6 h Rehabilitation Medic : 5 h

Physiology : 12 h Emergency Medicine : 2 h Radiology : 2 h Perinatologi : 3 h

History taking : Neurology 1 topic, Eye 1 topic, ENT 1 topic. Module discussion : Neurology 2 topic, Eye 1 topic, ENT, 1 topic, Psychiatry 1 topic, Pharmacology 4 topic (Pharmacology 3 classes) Skill Exam : Neurology 4 topic, Psychiatric 1 topic, Eye 2 topic, ENT 2 topic, Rehab Medic 1 topic, Emergency Medicine 1 topic. Time Period : 24 August – 04 December 2009 UTS 1 (Middle exam 1) : 12 October – 16 October 2009 UTS 2 (Middle exam 2) : 30 November – 04 December 2009 UAS (Remedial exam) : 28 December – 31 December 2009

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WEEK 3 WEEK 4

TIME Monday Tuesday Wednesday Thursday Friday Monday Tuesday Wednesday Thursday Friday 7-9-2009 8-9-2009 9-9-2009 10-9-2009 11-9-2009 28-9-2009 29-9-2009 30-9-2009 1-10-2009 2-10-2009

07.00 – 08.00


Public Health 1

Coma 1 Psychiatric 3 Sleep Disorder 1


08.00 – 09.00

Neuro Radiology 1

Neuro Oncology 1 dan 2

Psychiatric 1 Lecture Stroke 1

Public Health 2

Coma 2 Psychiatric 4 Sleep Disorder 2

09.00 – 10.00

Neuro Radiology 2

NS 1 Hydrocephalus

Psychiatric 2 Lecture Stroke 2

NS 4 ICH Spontan

Coma 3 Pharmacology Psychiatric 1

Entomology 5

10.00 – 11.00

Pathology Anatomy Neuro 1

NS 2 Meningokel

Neuro-Pharmacology 1

Lecture Stroke 3

NS 5 Head Trauma

Pharmacology Psychiatric 2

Entomology 6

11.00 – 12.00 Pathology Anatomy Neuro 2

NS 3 Brain Tumor

Neuro- Pharmacology 2

NS 6 Head Trauma

Pharmacology Psychiatric 3

Entomology 7

12.00 – 13.00 LUNCH BREAK LUNCH BREAK 13.00 – 14.00 Skill

Motoric Sensoric

Discussion Module Stroke

NON –

SISTEM SUBJECT

Skill CN, Reflexes & Psychiatry

Skill CN, Reflexes & Psychiatry

Rational Drug Therapy 6 Steps Epilepsy & Insomnia

NON –

SISTEM SUBJECT

14.00 – 15.00 15.00 – 15.30

Notes :



Physiology : 12 h Emergency Medicine : 2 h Radiology : 2 h


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WEEK 5 WEEK 6 WEEK 7 TIME Monday Tuesday Wednesday Thursday Friday

Middle Exam 1

or UTS 1

12 Oct until

16 Oct 2009

Monday Tuesday Wednesday Thursday Friday 5-10-2009 6-10-2009 7-10-2009 8-10-2009 9-10-2009 19-10-2009 20-10-2009 21-10-2009 22-10-2009 23-10-2009

07.00 – 08.00

Psychiatry 5

Neuro Emergency 1

Schizophrenia Neuro Degenerative


Anatomy Eye 1

Eye 1

Psychiatry 7 Headache 1


08.00 – 09.00

Psychiatry 6

Neuro Emergency 2

Schizophrenia Neuro Degenerative

Anatomy Eye 2

Eye 2 Psychiatry 8 Headache 2

09.00 – 10.00

Neuro Anaesthesi 1

Entomology 8

Schizophrenia Microbiology Eye 1

Physiology Eye 1

Eye 3 Forensic 1

Vertigo

10.00 – 11.00

Neuro Anaesthesi2

Entomology 9

Microbiology Eye 2

Physiology Eye 2

Eye 4 Forensic 2 Entomology 11

11.00 – 12.00

Entomology 10

Biochemic Eye

Forensic 3 Entomology 12

12.00 – 13.00 LUNCH BREAK 13.00 – 14.00 Emergency

Medicine 1 & 2

Discussion Module Schizophrenia

Skill MMSE Provocative


Pharmacology Eye 1 & 2

History Taking Eye

Skill Emergency Medicine

Skill Emergency Medicine


14.00 – 15.00 15.00 – 16.00

Notes :



Physiology : 12 h Emergency Medicine : 2 h Radiology : 2 h History taking : Neurology 1 topic, Eye 1 topic, ENT 1 topic. Module discussion : Neurology 2 topic, Eye 1 topic, ENT, 1 topic, Psychiatry 1 topic, Pharmacology 4 topic (Pharmacology 3 classes) Skill Exam : Neurology 4 topic, Psychiatric 1 topic, Eye 2 topic, ENT 2 topic, Rehab Medic 1 topic, Emergency Medicine 1 topic. Time Period : 24 August – 04 December 2009 UTS 1 (Middle exam 1) : 12 October – 16 October 2009 UTS 2 (Middle exam 2) : 30 November – 04 December 2009 UAS (Remedial exam) : 28 December – 31 December 2009

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WEEK 8 WEEK 9 TIME Monday Tuesday Wednesday Thursday Friday Monday Tuesday Wednesday Thursday Friday

26-10-2009 27-10-2009 28-10-2009 29-10-2009 30-10-2009 2-11-2009 3-11-2009 4-11-2009 5-11-2009 6-11-2009 07.00 – 08.00

Psychiatry 9 Eye 5

Neuro Pediatric 1

ENT 1


Eye 9

Neuro Trauma

Lecture Cataract 1

ENT 6


08.00 – 09.00

Psychiatry 10 Eye 6 Neuro Pediatric 2

ENT 2 Eye 10 Neuro imunology

Lecture Cataract 2

ENT 7

09.00 – 10.00

Anatomy ENT 1

Eye 7 Pediatric 1 Meningitis

ENT 3 Eye 11 Forensic 4

Lecture Cataract 3

ENT 8

10.00 – 11.00

Anatomy ENT 2

Eye 8 Pediatric 2 Meningitis

ENT 4 Eye 12 Forensic 5 Pediatric 4 Kejang demam

ENT 9

11.00 – 12.00 Pediatric 3 Ensephalitis

ENT 5 Forensic 6 Pediatric 5 Epilepsi

ENT 10

12.00 – 13.00 LUNCH BREAK 13.00 – 14.00 Entomology

13 & 14 Perinatologi

1,2,3 History Taking ENT


Discussion Cataract

Skill Eye 1 & ENT 1

Skill Eye 1 & ENT 1


14.00 – 15.00 15.00 – 16.00

Notes :




History taking : Neurology 1 topic, Eye 1 topic, ENT 1 topic. Module discussion : Neurology 2 topic, Eye 1 topic, ENT, 1 topic, Psychiatry 1 topic, Pharmacology 4 topic (Pharmacology 3 classes) Skill Exam : Neurology 4 topic, Psychiatric 1 topic, Eye 2 topic, ENT 2 topic, Rehab Medic 1 topic, Emergency Medicine 1 topic. Time Period : 24 August – 04 December 2009 UTS 1 (Middle exam 1) : 12 October – 16 October 2009 UTS 2 (Middle exam 2) : 30 November – 04 December 2009

UAS (Remedial exam) : 28 December – 31 December 2009

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9-11-2009 10-11-2009 11-11-2009 12-11-2009 13-11-2009 16-11-2009 17-11-2009 18-11-2009 19-11-2009 20-12-2009 07.00 – 08.00

Eye 14 Neuropathy 1 Psychiatry 11 ENT 11


Eye 18 Entomology 17

Psychiatry 13 ENT 16


08.00 – 09.00

Eye 15 Neuropathy 2 Psychiatry 12 ENT 12 Eye 19 Entomology 18

Psychiatry 14 ENT 17

09.00 – 10.00

Eye 16 NS 7 Spinal cord and Root Compressions

Pharmacology ENT 1

ENT 13 Eye 20 Entomology 19

Microbiology ENT 1

ENT 18

10.00 – 11.00

Eye 17 NS 8 Lumbar Disc Protrussion

Pharmacology ENT 2

ENT 14 Eye 21 Entomology 20

Microbiology ENT 2

ENT 19

11.00 – 12.00 NS 9 Kelainan Saraf Tepi

ENT 15 ENT 20

12.00 – 13.00 LUNCH BREAK LUNCH BREAK 13.00 – 14.00 Entomology

15 & 16 Pathology Anatomy ENT 1 & 2

Rational Drug Therapy 6 Steps Eye & ENT


Skill Eye 2 & ENT 2

Skill Eye 2 & ENT 2


14.00 – 15.00 15.00 – 16.00

Notes :





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23-11-2009 24-11-2009 25-11-2009 16-11-2009 27-11-2009 30-11-2009 1-12-2009 2-12-2009 3-12-2009 4-12-2009 07.00 – 08.00

Eye 22 Movement Disorder 1

Skill Evaluation Lecture Hearing Loss 1

Middle Exam 2 UTS 2

30 November until 04 December 2009

08.00 – 09.00

Eye 23 Movement Disorder 2


09.00 – 10.00

Eye 24 Rehabilitation Medic 1


10.00 – 11.00

Eye 25 Rehabilitation Medic 2

Skill Evaluation

11.00 – 12.00 Rehabilitation Medic 3

Skill Evaluation

12.00 – 13.00 LUNCH BREAK 13.00 – 14.00 Skill

Rehab Medic Skill Rehab Medic

Discussion Hearing Loss

14.00 – 15.00 15.00 – 16.00

Notes :

Green colour : Lecture; Purple : Discussion / Skill; Blue : Lunch break; Yellow: Self study; Black: Holiday Lecture : 3 classes (Class A: R.K.I ; Class B: R.6.04; English class: R.4.08) Discussion & Skill : 12 small classes (R.K.I, R.6.04, R.4.08, R.2.01 – R.2.07, R.3.10 - R.3.11) Laboratory involved : Neurology : 33 h Anatomy Histology : 10 h Parasitology : 2 h Biochemic Eye : 1 h




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List Topic Kuliah Non Modul : Neurologi Block IX ; Semester V ; Tahun Ajaran 2009‐2010

No Hari / Tanggal Jam Topic Nama Pengajar

KB Inggris Reg A Reg B

1 Senin, 24‐8‐09 08.00 – 09.00 Overview SNK MRA WMS

2 Selasa, 25‐8‐09 08.00 – 10.00 Basic Neurology SNK MRA MDH

3 Kamis, 27‐8‐09 08.00 – 10.00 Epilepsy BBS SBR WMS

4 Kamis, 3‐9‐09 08.00 – 10.00 Meningitis EKA HRP SBR

5 Selasa, 8‐9‐09 08.00 – 09.00 Neuro Onkologi EKA SBR WMS

6 Kamis, 10‐9‐09 08.00 – 11.00 Stroke HRP EKA MDH

7 Selasa, 28‐9‐09 07.00 – 10.00 Coma SNK WMS MDH

8 Kamis, 1‐10‐09 07.00 – 09.00 Sleep Disorder HRP MRA WMS

9 Selasa, 6‐10‐09 07.00 – 09.00 Neuro Emergency EKA SNK BBS

10 Kamis, 8‐10‐09 07.00 – 09.00 Neuro Degenerative WMS MRA SBR

11 Kamis, 22‐10‐09 07.00 – 09.00 Headache SNK HRP EKA

12 Rabu, 28‐10‐09 07.00 – 09.00 Neuro Pediatric BBS WMS SBR

13 Selasa, 3‐11‐09 07.00 – 09.00 Neurotrauma & munologi BBS SBR SNK

14 Selasa, 10‐11‐09 07.00 – 09.00 Neuropati SNK MDH MRA

15 Selasa, 23‐11‐09 07.00 – 09.00 Movement Disorder HRP MDH WMS

HRP : dr .Hari Purnomo SpS(K) SBR : dr. SB Rianawati SpS MDH : dr. M Dalhar SpS(K) EKA : dr. Eko Arisetijono SpS BBS : dr. Bambang Budiarso SpS(K) SNK : dr. Shahdevi NK SpS MRA : dr. Masruroh Rahayu MKes WMS : dr. Widodo SpS

14

List Topic Kuliah Non Modul : EAR, NOSE THROAT Block IX ; Semester V ; Tahun Ajaran 2009‐2010

TIME TOPIC TITLE TUTOR

WEEK 8

Thursday, 29.10.2009

ENT 1, 2, 3, 4, 5 Ear 1. J. Bambang Soemantri, dr, SpTHT‐KL(K).

2. H. Edi Handoko, dr, SpTHT‐KL.

3.Dyah Indrasworo, dr, SpTHT‐KL.

History Taking ENT History Taking

1. Soehartono, dr, SpTHT‐KL.


3. Hendradi Surjotomo, dr, SpTHT‐KL. + PPDS THT senior

WEEK 9


ENT 6, 7, 8, 9, 10

Nose 1. Rus Suheryanto, dr, SpTHT‐KL(K).

2. Endang Retnoningsih, dr, SpTHT‐KL(K).


Wednesday, 04.11.2009

Skill examination

ENT examination 1





Skill examination

ENT examination 1




WEEK 10


ENT 11, 12, 13, 14, 15

Pharyx 1. H. Lukmantya, dr, SpTHT‐KL(K).

2.Dr. Pudji Rahaju, dr, SpTHT‐KL(K).


WEEK 11


ENT 16, 17, 18, 19, 20

Larynx 1. H. Lukmantya, dr, SpTHT‐KL(K).

2.Dr. Pudji Rahaju, dr, SpTHT‐KL(K).



Skill examination

ENT examination 2





Skill examination

ENT examination 2





Skill examination

ENT skill evaluation




15

List Topic Kuliah Non Modul : Ear, Nose, & Throat Block IX ; Semester V ; Tahun Ajaran 2009‐2010

TIME TOPIC TITLE TUTOR

WEEK 12


ENT modul discussion

Hearing loss 1. J. Bambang Soemantri, dr, SpTHT‐KL(K).


3. Dyah Indrasworo, dr, SpTHT‐KL. + tutor lain


ENT module lecture (hearing impairment)

Hearing loss 1. J. Bambang Soemantri, dr, SpTHT‐KL(K).


3. Dyah Indrasworo, dr, SpTHT‐KL.

16

List Topic Kuliah Non Modul : Anatomi‐Histologi Block IX ; Semester V ; Tahun Ajaran 2009‐2010

Hour Literacy Time Frame A Class B Class English Class

1

August 24th 2009

09.00 – 09.50 5 1

2 10.00 – 10.50 3 2

3 11.00 – 11.50 4 5

4

August 31st 2009

08.00 – 08.50 6 3

5 09.00 – 09.50 1 4

6 10.00 – 10.50 2 6

UTS 1 ; October 12th – 16th 2009

7 October 19th 2009

07.00 – 07.50 7 9

8 08.00 – 08.50 8 10

9October 26th 2009

09.00 – 09.50 9 7

10 10.00 – 10.50 10 8

Lecturer Topic

Code Content

Andi Ansharullah, dr, DAAK. 1

Organization of the Nervous System : Central Nervous System (CNS)

2 Vascular System of the Brain & Cerebrospinal Fluid

Dr. med. Tommy Alfandy Nazwar, dr. 3 Peripheral Nervous System (PNS)

4 Autonomic Nervous System (ANS)

Bambang Sumantri, dr, MKes. 5 Histology of the CNS

6 Histology of the PNS & ANS

Danik Agustin, dr, MS. 7 Anatomy of the Eye

8 Anatomy of the Ear, Nose & Throat

Djoko Santoso, dr, MKes. 9 Histology of the Eye

10 Histology of the Ear, Nose and Throat

17

List Topic Kuliah Non Modul : Farmakologi Block IX ; Semester V ; Tahun Ajaran 2009‐2010

No Hari / Tanggal

Jam Topic Nama Pengajar

KB Inggris Reg A Reg B

1 Rabu,

9‐9‐2009 10.00 – 12.00

Neurotransmission & CNS Drug for epilepsy & seizures Analgesic & antiinflammaory drug

Prof. Aris Widodo, dr, MS, SpFK, PhD.

Dr. Setyawati SK, dr, MKes.

Dr. Nurdiana, dr, MKes.

2 Rabu,

30‐9‐2009 09.00 – 12.00

Hypnotics & sedatives Antidepressant, antianxiety Antimanic Anti Parkinson Drug abuse

Prof. Aris Widodo, dr, MS, SpFK, PhD.



3 Senin,

19‐10‐2009 13.00 – 15.00

Chemotherapy of microbial Autonomic agents Analgesic & antiiflammatoryLocal anaesthetics In ophthalmic procedures


Dr. Nur Permatasari, drg, MS.


4 Rabu,

11‐11‐2009 09.00 – 11.00

Chemotherapy of microbialAutonomic agents Antiistamines Analgesic & antiiflammatoryReview anti cancer


Dr. Nur Permatasari, drg, MS.


18

List Topic Kuliah Non Modul : Mikrobiologi Block IX ; Semester V ; Tahun Ajaran 2009‐2010

Microbiology CNS

Polyomyelitis, Rabies, Tetanus, Botulism 1. Prof.Dr.dr.Sumarno,SpMK.

2. Dr.Sri Winarsih,Apt.,MSi.

3. dr.Roekistiningsih, MS,SpMK

Class A

Class B

Class English

Microbiology Eye

Keratitis herpes, Bacterial & Viral Conjuctivitis, Trachoma, Hordeolum

1. Dr.drh.Sri Murwani, MP

2. Prof.Dr.dr.Noorhamdani,SpMK

3. Prof. Dr.dr.Sanarto Santoso,SpMK

Class A

Class B

Class English

Microbiology ENT

Difteri, Streptococcal shore throat, Viral pharingytis, Otitis media (acute & chronic)

1. Dr.Sri Winarsih, Apt.MSi

2. dr. Roekistiningsih, MS.,SpMK

3. Prof.Dr.dr.Sumarno,SpMK.

Class A

Class B

Class English

19

A Brief Review of Neuroanatomy This very selective review focuses on aspects of neuroanatomy that are of particular clinical importance. Much of this will be familiar, since your were exposed to neuroanatomy in much greater detail last year in Neuroscience.

1. The Spinal Cord 2. The Brain Stem And Cerebellum 3. The Diencephalon 4. The Basal Ganglia 5. The Cerebral Cortex 6. The Peripheral Nervous System, Neuromuscular Junction, and Muscle

1.The Spinal Cord The spinal cord is the simplest portion of the central nervous system, with the same general structure (with variations that we will ignore) at every segmental level.

Anatomy It is important to understand the distinction between segmental and long tract findings.

1. The segmental level: a. At each segment, sensory neurons contained in a dorsal root enter the spinal

cord. The territory of skin innervated by a segment (for example, C6) is called a dermatome.

b. Motor neuron cell bodies are located in the anterior horns; for each segment, their axons collect to form an anterior spinal root, and project (via plexus and peripheral nerves) to groups of muscles (the myotome).

c. Large sensory fibers from muscle spindles enter at each level and synapse with motor neurons that project to the same muscle. The monosynaptic stretch reflex arc is an important aspect of segmental organization.

2. Long tracts: of the 10 or more long fiber tracts coursing longitudinally in the spinal cord, only three are of prime importance in clinical practice:(see Figure 1) below :

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a. The lateral corticospinal tract contains axons from neurons in the motor cortex that project directly or through interneurons to motor neurons at the segmental levels

b. Sensory fibers subserving pain and temperature (and crude touch) enter at each segment through the dorsal roots, synapse, and the second order neuron crosses to join the spinothalamic tract.

c. Sensory fibers subserving position, vibration and disciminative touch enter through the dorsal roots, and directly (without a synapse and without crossing) join the posterior (or dorsal) columns

d. Autonomic function: Autonomic fibers descend and synapse with cell bodies in the intermediolateral columns. Sympathetic fibers exit between T1 and L2, and parasympathetic between S2 and S4.

Localization Spinal cord lesions are suspected when there are long tract signs below a certain spinal level, with or without segmental signs at that level

1. Segmental signs: a. Motor: weakness and atrophy in a myotomal pattern. b. Sensory:

1. Sensory loss in a dermatomal distribution. 2. With central cord lesions: bilateral dissociated sensory loss (loss of

pain and temperature, with preservation of position, vibration and touch.

3. Reflexes: loss of tendon reflexes at the level of the lesion. 2. Long tract signs:

a. Motor: upper motor neuron dysfunction is characterized by weakness, spasticity, increased tendon reflexes, and Babinski responses. Bilateral leg weakness (paraparesis) is the commonest presentation of spinal cord dysfunction, but quadriparesis, monoparesis or any combination of limb weakness can be seen. Acute transection (or similarly severe lesion) can cause

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Aspinal shock,@ with flaccid paralysis and diminished tendon reflexes. This is temporary: spastic paralysis will usually supervene.

b. Sensory: The characteristic finding is that of bilateral sensory loss below the level of the lesion. When spinal cord pathology is suspected, the physical examination should be designed to detect sensory levels in the limbs and on the trunk. The modalities lost depend upon the tracts involved.

c. Autonomic: Many autonomic functions can be affected, but clinically the most useful symptoms relate to bladder control. Loss of descending inhibition of segmental reflex control leads to urinary urgency and incontinence. Acutely, however, lesions may be associated with a flaccid bladder and urinary retention, be�� segmental reflexes become active.

3. Classic syndromes:

The Brown-Sequard syndrome of spinal cord hemisection (see figure 2) below :

Segmental findings with spinal cord hemisection will depend upon the level of the lesion and its rostro-caudal extent: they may be totally inapparent, for example, with a small lesion in the thoracic cord. Long tract findings, however, are prominent. Posterior column sensory loss (position, vibration) and long tract motor signs are found ipsilateral to the lesion, whereas pain and temperature are lost contralaterally. Bladder function may be spared since bilateral lesions are required to interfere with bladder function.

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Extrinsic compression Extrinsic spinal cord compression from neoplasms or other masses affects the spinal cord by direct compression and by interference with blood supply. Segmental findings are variable, and again depend on the level and extent of the lesion. If nerve roots are affected, segmental motor, sensory, or reflex changes may be apparent at the level of the lesion (see number 4 below, spondylotic myelopathy). Sometimes, these are minimal. The long tract findings are clinically more important, since they indicate that there is spinal cord, rather than just nerve root, involvement. The lateral columns and intermediolateral columns are particularly prone to damage, so urinary urgency and lower extremity long tract motor signs are often the earliest manifestation of spinal cord compression. Loss of pain and temperature sensation may begin in the sacral region, and slowly ascend as the compression gets more severe, because the spinothalamic tract is laminated with the fibers from the sacral regions being most lateral and thus most vulnerable to compression. Central cord syndrome (see figure 3) below :

If a lesion in the center of the spinal cord extends over many segmental levels, segmental findings are prominent. Intrinsic spinal cord neoplasms and cysts (syringomyelia) may present with segmental loss of pain and temperature sensation, loss of tendon reflexes, segmental atrophy and weakness, and, below the level of the lesion, long tract signs (spasticity, brisk reflexes, Babinski response, weakness,

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urinary urgency, and, later, long tract sensory abnormalities). If the process begins in the middle of the cord, the first manifestation will be a dissociated sensory loss (loss of pain and temperature without loss of position and vibration) resulting from interruption of second order sensory neurons decussating in the center of the cord on their way to the lateral spinothalamic tracts. With cervical syringomyelia (a cyst in the cervical spinal cord), the dissociated sensory loss is usually bilateral, and may assume a cape distribution. Cervical spondylotic myelopathy Degenerative changes in the cervical spine (disc degeneration, formation of new bone) may impinge on spinal roots and may also compress the spinal cord. A common presentation is with C6 segmental findings (particularly decreased biceps and brachioradialis reflexes) and long tract abnormalities below that level (with increased triceps and lower extremity reflexes, spasticity in the legs, Babinski responses, and urinary urgency). Sensory findings, both segmental and long tract, may be present, but tend to be a later complication.

2.The Brain Stem and Cerebellum Long tracts Long tracts: the motor and sensory tracts described in the spinal cord are present in the brain stem, but in the brain stem they are all contralateral to the side of the body they serve.

1. The pyramidal tract (upper motor neuron) is located in the cerebral peduncles of the midbrain, it courses through the base of the pons in several bundles that rejoin to form the pyramids in the medulla. The pyramids decussate at the junction of the medulla and cervical spinal cord. See figure 4 below :

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2. The spinothalamic tracts continue in a lateral position throughout the brainstem on their way to the thalamus (figure 5).

3. The posterior columns end in the medulla where they synapse in the nuclei cuneatus and gracilis (subserving function in the arms and legs respectively). Second order neurons immediately decussate to form the medial lemnisci. The medial lemnisci are medially situated in the medulla, but in the pons they become horizontally oriented and by the midbrain they are situated laterally, near the spinothalamic tracts. These sensory pathways both end in the thalamus (VPL). (figure 5). Below :

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Segmental structures The segmental anatomy of the brainstem is analogous to that of the spinal cord, but it is more complex. We will not attempt to describe brainstem anatomy in detail: please consult your neuroscience notes and texts for details. figure 6 below , illustrates the approximate location of brainstem sensory and motor nuclei and Table 1 is a rough guide to segmental level.

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Level Nuclei

Midbrain III, IV, mesencephalic V

Pons V (main nucleus)

Caudal pons VI, VII

Ponto‐medullary junction VIII

Medulla

N. of the descending tract of V.N. ambiguusN. tractus solitariusMotor X

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XII

Cervical cord XI

With the exception of the trochelar nucleus (cranial nerve IV), which crosses to innervate the contralateral superior oblique muscle, each of the brainstem cranial nerve nuclei innervate ipsilateral structures. Since the long tracts discussed above are crossed, lesions confined to one side of the brainstem typically present with cranial nerve findings on one side, and motor and sensory findings on the opposite side of the body. This rule is very helpful in localization. (See section II-G below, and figure 7, figure 8and figure 9, for examples.)

The reticular formation Although typically thought of as an amorphous background in which brainstem nuclei are arranged, the reticular nuclei and tracts form a complex and detailed structure with diverse functions. In the medulla and pons, reticular nuclei are important in modulating respiration, heart rate and blood pressure. The reticular formation of the rostral pons and midbrain is critical for the maintenance of consciousness (lesions in this area result in coma), and reticular nuclei (such as the PPRF) are important for mediating eye movement. Some brainstem nuclei provide a major source of particular neurotransmitters for large portions of the brain: the locus coeruleus (norepinephrine), the raph nuclei (serotonin), and the substantia nigra (dopamine). These neurotransmitters are important neuromodulators. Reduction in norepinephrine or serotonin probably affects arousal and emotion. Neurological correlates are clearer for dopamine: Parkinsons disease is associated with loss of dopaminergic pigmented neurons in the substantia nigra.

The cerebellum Lesions of one cerebellar cortex result in ataxia on the same side as the lesion. The cerebellar hemisphere projects to the dentate nucleus of the cerebellum, whose fibers leave the cerebellum in the superior cerebellar peduncle, cross as soon as they reach the brain stem, and synapse in the contralateral red nucleus and thalamus (VA and VL). Collateral fibers from the corticospinal tract synapse in the basis pontis, and fibers from these pontine nuclei project to the opposite cerebellar hemisphere. Thus, for example, the right cerebellar hemisphere projects to the left thalamus and cortex, which in turn projects to the left pontine nuclei, which project back to the right cerebellar hemisphere.

The control of eye movements.

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Horizontal eye movements (see Figure 7):

a. Anatomy A conjugate horizontal eye movement requires simultaneous activation of one lateral rectus muscle and the contralateral medial rectus muscle. The sixth nerve nucleus contains motor neurons that control the lateral rectus muscle. It also contains neurons that project through the medial longitudinal fasciculus (MLF) to the medial rectus subnucleus of the contralateral third nerve nucleus. This subnucleus contains motor neurons that control the medial rectus muscle. Thus activation of the sixth nerve nucleus can cause a conjugate lateral eye movement toward the side of the nucleus stimulated.

b. "Voluntary" horizontal eye movements can be directed by the frontal eye fields. Stimulation of the frontal eye field on one side causes deviation of the eyes to the opposite side. To achieve this, the frontal eye fields are connected with the contralateral pontine lateral gaze center (the paramedian pontine reticular formation or PPRF), the pathway crossing in the caudal midbrain.

c. Clinical correlation: Horizontal gaze palsy: Paresis of conjugate eye movements is called a gaze palsy. Horizontal gaze palsy may be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion, or from brain stem lesions,

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which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion. Another way to remember this is that patients with hemisphere lesions look toward their lesion, while patients with pontine gaze palsies look away from their lesions. Note that patients with gaze palsy still have conjugate eye movements and therefore do not complain of diplopia. Internuclear ophthalmoplegia: Lesions of the medial longitudinal fasciculus (MLF) between the sixth and third nerve nuclei cause weakness of adduction on attempts at horizontal gaze, but not with convergeance. For example, a lesion of the right MLF will cause weakness of adduction of the right eye on attempted leftward gaze. One can demonstrate that this weakness is not caused by medial rectus paralysis, because this muscle functions normally during convergeance (which is coordinated entirely in the midbrain).

d. Vertical eye movements: These are coordinated in the midbrain. There are centers for vertical gaze in the mesencephalic reticular formation just above the third nerve nuclei.

Influence on posture Brain stem lesions can affect numerous descending influences on the motor system. Tectospinal, reticulospinal and vestibulospinal pathways influence axial muscle tone and movement. In contrast, corticospinal and rubrospinal pathways innervate limb muscles more than axial muscles. The corticospinal pathways are phylogenetically newer, and mediate the most highly differentiated limb movements, such as individual finger movements. Lesions that upset the balance among these systems can produce abnormal posturing.

Lesions in the brain stem above the pontomedullary junction can result in disinhibition of lateral vestibulospinal and caudal reticulospinal systems that normally promote extensor tone in all extremities. The result is extensor posturing in all extremities (decerebrate posturing). Lesions above the brain stem that interfere with cortical and basal ganglia modulation of all brain stem motor systems may result in decorticate posturing, in which there is flexion of the upper extremities and extension of the lower extremities. Flexor tone in the upper extremities is probably mediated at least in part by rubrospinal and reticulospinal pathways.

Classic syndromes The following are examples of brainstem syndromes. You are not responsible for knowing the names of these syndromes, but you should try to understand how these lesions are localized.

Midbrain syndromes: Weber's syndrome (see Figure 8)

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The critical structures involved are the descending corticospinal and corticobulbar fibers in the cerebral peduncle, and the fibers of the third nerve that traverse the peduncle on exiting the midbrain. With a lesion on the right, the patient will have a left hemiparesis and a right third nerve palsy (ptosis, inability to move the eye up, down or medially, and [if fibers from the Edinger‐Westphal nucleus are involved] pupillary dilitation).

Benedikt's syndrome

unilateral third nerve palsy with contralateral ataxia, from a midbrain stroke involving the third nerve as it travels near the red nucleus. A lesion of the red nucleus interrupts fibers from the opposite cerebellar hemisphere (dentate nucleus of the cerebellum superior cerebellar peduncle crossing in midbrain red nucleus VA/VL thalamus).

Medial pontine syndromes

Lesions of the sixth nerve nucleus cause paralysis of gaze to the side of the lesion. If fibers from the opposite 6th nerve nucleus are involved as they cross to the MLF, there is also weakness of the ipsilateral medial rectus muscle. The ipsilateral seventh nerve can be involved since its fibers course around the sixth nerve nucleus. Lesions involving the fibers of the sixth nerve as they travel through the pons can also involve the medial lemniscus (producing unilateral abducens weakness and contralateral loss of position and vibration), or descending corticospinal fibers in the base of the pons (producing unilateral abducens weakness and contralateral hemiparesis).

Lateral medullary syndrome (Wallenberg syndrome)

This is the commonest of the brain stem strokes. Involvement of the spinothalamic tract results in contralateral loss of pain and temperature sensation below the neck.

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Involvement of the descending nucleus and tract of V results in loss of pain and temperature sensation on the face ipsilateral to the lesion. Involvement of descending autonomic fibers results in an ipsilateral Horner's syndrome (ptosis, meiosis, and anhidrosis). Involvement of the nucleus ambiguus causes palatal weakness and dysphagia. Involvement of the inferior cerebellar peduncle (restiform body) causes ipsilateral ataxia. See figure 9.

The locked in syndrome (infarction of the base of the pons)

Corticospinal and corticobulbar tracts in the basis pontis are interrupted, causing quadriplegia and paralysis of all cranial nerve muscles except for those controlling eye movements. If the lesion extends into the tegmentum of the caudal pons, horizontal eye movements may also be affected (so only vertical eye movements are possible), and sensation can be affected. The critical feature of these lesions is that they spare the reticular formation above the caudal pons, and therefore the patients remain awake. The only way to communicate with these unfortunate patients is to ask them to move their eyes in response to questions.

Pontine hemorrhage

Hemorrhage into the pons (usually the result of hypertensive vascular disease) results in coma (from involvement of the reticular formation), decerebrate posturing (lesion between red nucleus and vestibular nucleus), and small pupils (involvement of descending sympathetic fibers).

3.The Diencephalon

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The diencephalon consists of the thalamus, hypothalamus, subthalamus, and epithalamus. The subthalamus is considered with the basal ganglia (below). Lesions of the epithalamus (habenula) have not been correlated with specific deficits in man, possibly because isolated lesions have not been described.

The thalamus

This complex structure figure 10serves to process all sensory input (except olfactory) to the cortex, but it also has profound influence on motor (via input from basal ganglia and cerebellum) and cognitive function. Although critically situated, the functions of the thalamus are not well understood.

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We will mention only the most well-defined clinico-pathologic correlations:

Sensory function:

• Visual input from the optic tract relays in the lateral geniculate nucleus (LGN): lesions result in hemianopia (see figure 11) as below :

• Auditory input from the lateral lemniscus relays in the medial geniculate nucleus. Unilateral lesions have little effect on hearing, because auditory information from each ear ascends bilaterally.

• Somatosensory input from both the posterior column/medial lemniscus system for position and vibration and the spinothalamic system for pain and temperature relay in the thalamus (VPL and VPM nuclei). Lesions affecting this part of the thalamus can therefore cause loss of all sensation on one side of the body. Paradoxically, some patients experience abnormally painful sensations (Athalamic pain@) on the anesthetic side.

Motor function

Thalamic strokes are not known for their motor manifestations, but interruption of the cerebellar input to VA and VL may result in ataxia, and interruption of basal ganglia input (to these same thalamic nuclei, VA and VL) may result in akinesia.

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Cognitive function:

• Arousal: bilateral lesions affecting the intralaminar thalamic nuclei, which can be considered extensions of the brainstem reticular formation, can cause unresponsiveness, but the eyes remain open. This has been called coma vigil or akinetic mutism.

• Memory: Lesions affecting medial thalamic structures (the confluence of mammillothalamic and amygdalofugal tracts, dorsomedial and possibly anterior nuclei) can cause profound amnesia.

• Other cognitive functions: aphasia, neglect and visuospatial dysfunction have been described with thalamic lesions, and presumably relate to interruption of reciprocal thalamic connections with the cerebral cortex.

The hypothalamus The hypothalamus exerts control over the pituitary gland and thus over endocrine function in general, and it has extensive connections with brainstem autonomic nuclei. Lesions of the hypothalamus affect appetite, emotional behavior, temperature control, and numerous other autonomic and endocrine-influenced behaviors.

4.The Basal Ganglia The basal ganglia are a group of anatomically closely related subcortical nuclei. Damage to these nuclei does not cause weakness, but can cause dramatic motor abnormalities. The mechanisms by which lesions in the basal ganglia cause clinical symptoms have not been completely elucidated.

Anatomy (see figure 08) The striatum (caudate and putamen) receives projections from wide regions of the neocortex, and projects to the globus pallidus (GP). The nucleus accumbens and the ventral pallidum (vP) are limbic regions of the caudate and GP, respectively (figure 12) as follows :

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The striatum also projects to and the pars reticulata of the substantia nigra (SNpr), which is not shown in the illustrations. SNpr and GPi are closely related structures with similar connections. The globus pallidus and SNpr projects to the thalamus (VA/VL), which projects back to cortex. In addition to a motor loop shown in detail in figure 13 :

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that projects to motor cortical structures , several other cortico-striato-pallido-thalamic-cortical loops have been defined anatomically (two are shown in figure 14, the dorsolateral frontal and orbitofrontal (limbic) loops) :

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Additionally, there is a sub-circuit from the globus pallidus to the subthalamic nucleus, and back to the globus pallidus shown in Figure 13.

Clinical syndromes: Parkinsonism

Loss of dopaminergic neurons in the substantia nigra (pars compacta) that normally project to the striatum is associated with rigidity, bradykinesia, tremor, and loss of postural reflexes. that characterize Parkinson's disease.

Hemiballismus (hemichorea) Hemiballismus is associated with damage to the contralateral subthalamic nucleus of Luys.

Huntington's chorea an hereditary disease characterized by progressive dementia and chorea, is associated with atrophy of the caudate nucleus. Strokes of the caudate, however, rarely cause chorea.

5.The Cerebral Cortex The primary sensory and motor areas You should know where primary visual, auditory, somatosensory and motor cortices are located:See figure 15.:

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1. The visual (striate) cortex (calcarine cortex, occipital lobes, area 17) Take time to review the visual pathways: retina optic nerve optic chiasm optic tract lateral geniculate body optic radiations visual cortex). Note that anterior to the optic chiasm, unilateral lesions produce visual deficits in only one eye, whereas posterior to the chiasm, deficits are restricted to one visual field (but are present in both eyes). See figure 11.

2. The auditory cortex (Heschl's gyrus, temporal lobe, within the Sylvian fissure). 3. The somatosensory cortex (post‐central gyrus, areas 3,1 and 2).

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4. The motor cortex (pre‐central gyrus, area 4).

Association cortex: 1. Unimodal association cortex: Each of the primary sensory cortices is bordered by

unimodal association cortex (that is, with direct connections to only one sensory modality).

2. Polymodal and supramodal association cortices are interconnected with unimodal association areas as well as other higher‐order association cortices. Function is thought to depend upon complex networks of neurons in multiple regions; nevertheless, very specific functions are subserved by different regions. Some regions are specialized for specific language functions, others for visuospatial, etc.

3. Prefrontal cortex: The expanse of cortex anterior to the motor and pre‐motor areas subserves Aexecutive@ functions. Patients with frontal lobe damage may have difficulty using information not immediately at hand to direct behavior. They therefore exhibit poor planning and judgement (see below).

Cerebral dominance The two cerebral hemispheres are not functionally equivalent. The following functional asymmetries have been well-documented:

Language

In over 95% of right‐handers, the left hemisphere is dominant for language. In left handers, either left hemisphere dominance or bilateral language capabilities are the commonest findings; right hemisphere dominance is also described.

Handedness/praxis

Handedness reflects a functional hemispheric asymmetry for fine motor ability. Limb apraxia results from damage to the hemisphere opposite the dominant hand (e.g., the left hemisphere, in right‐handers).

Attention

Severe unilateral neglect is seen much more often with right than with left hemisphere damage, reflecting (it is thought) a functional hemispheric asymmetry of attentional mechanisms.

Visuospatial abilities

Certain visuospatial skills are more highly developed in the right hemisphere.

Emotion

While the exact nature of this asymmetry remains to be defined, the emotional effects of left hemisphere damage appear to be different from those of right hemisphere damage. Left frontal lesions are more likely to be associated with

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depression, whereas right hemisphere damage is more likely to cause emotional flattening.

Limbic cortex: emotion and memory. Anatomy (see figure 16)

Limbus means rim. Structures of the limbic cortex form a ring around the brainstem and diencephalon. Limbic structures include (going in a circle) the amygdala, hippocampus and parahippocampal gyrus, cingulate cortex, orbitofrontal, and insular cortex. Limbic regions tend to have a more primitive structure than neocortex, and are highly interconnected with basal forebrain and hypothalamus.

Function: Emotion

Emotional behavior entails endocrine, autonomic and motor changes regulated by the hypothalamus. Because the limbic forebrain is interposed between neocortex and hypothalamus, it is logical to suppose that it mediates cortical influence over

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hypothalamic function. Clinical and experimental data confirms this for a portion of the limbic forebrain: in animals, lesions of the orbitofrontal and temperopolar cortex, and of the amygdala, are associated with changes in emotional behavior. In humans, seizures arising from medial temporal structures (especially the amygdala) can be manifested by emotional feelings such as fear.

Memory

Lesions affecting the hippocampus and its connections do not appear to affect emotions, but instead can profoundly affect memory. Discrete lesions in the following structures can cause isolated and profound memory disturbances:

• the hippocampus and adjacent temporal cortex (entorhinal and perirhinal cortex).

• the medial thalamus (anterior thalamus, mamillothalamic tract, dorsomedial thalamus)

• the basal forebrain, perhaps especially the cholinergic neurons of the septal nuclei the diagonal band of Broca that project to the hippocampus. Other structures in this complex area may also contribute to memory.

Clinical syndromes Only a few will be mentioned.

The Aphasias (see Figure 17)

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Aphasia is most often associated with damage to left hemisphere cortex. The following distinctions are useful:

Summary of the aphasias

Syndrome Spont. Speech Comprehension Repetition Naming

Perisylvian aphasias

Broca's Non‐fluent ("Telegraphic") Good Poor Poor

Wernicke's Fluent (phonemic paraphasias) Poor Poor Poor

Conduction Fluent (phonemic paraphasias) Good Poor Poor

Global Non‐fluent Poor Poor Poor

Trans‐cortical aphasias

Transcortical motor Non‐fluent Good Good Var.

Transcortical sensory Fluent (semantic paraphasias) Poor Good Poor

Mixed Transcortical Non‐fluent Poor Good Poor

Anomic Fluent (circumlocution..) Good Good Poor

The perisylvian aphasias

Structures around the sylvian fissure mediate auditory language repetition. Auditory signals are processed by Heschl's gyrus (primary auditory cortex), and phonemic analysis probably takes place in the adjacent auditory association cortex (Wernicke's area). Speech is encoded by more anterior regions (among them, Broca's area, in front of the motor cortex), and these regions direct the adjacent motor cortex to produce the appropriate movements. Damage to any of these regions impairs language repetition, the hallmark of the perisylvian aphasias. Language comprehension requires that the phonetically analyzed information be communicated to regions outside the perisylvian region (among them, the angular gyrus).

Broca's aphasia

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Characterized by non‐fluent speech, poor repetition and relatively spared comprehension. Lesions are in Broca's area and adjacent cortex.

Wernicke's aphasia

Fluent, but nonsensical speech with phonemic paraphasias (substitution of incorrect sounds), and impaired repetition and comprehension. Lesions are in Wernicke's area.

Conduction aphasia

Fluent speech, spared comprehension, and poor repetition. Lesions may disconnect Wernicke's from Broca's area.

Global aphasia

Non‐fluent speech, poor repetition and poor comprehension. The entire perisylvian cortex is involved.

The transcortical aphasias

These are characterized by intact repetition. Lesions are more varied than with perisylvian aphasias. In addition to the cortical localizations noted, transcortical aphasias may result from subcortical damage.

Transcortical motor aphasia

Speech is non‐fluent, but repetition and comprehension are spared. Lesions are frontal, but spare Broca's area.

Transcortical sensory aphasia

Speech is fluent, but empty, and often semantic paraphasias (substitutions of incorrect words) are found. Comprehension is impaired, but repetition is normal. Lesions are posterior, but spare Wernicke's area.

Anomic aphasia

This can be conceived of as a mild transcortical sensory aphasia, in which comprehension is not affected, but naming is impaired. Speech is fluent, with circumlocution (when the patient cannot find a word). Repetition is normal. Angular and middle temporal gyrus lesions, as well as other areas, have been implicated.

Mixed transcortical aphasia

Non‐fluent speech, with poor comprehension, but normal repetition. Patients may echo fragments of other's speech (echolalia). Lesions usually encompass thos of both transcortical motor and transcortical sensory aphasias, and are most often from watershed infarctions associated with severe carotid artery stenosis.

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Disconnection syndromes

Neurological deficits may result not only from destruction of cortical regions that subserve specific functions, but also from disconnections between these areas. An example is the syndrome of alexia without agraphia (pure word blindness, Djerine's syndrome). Most commonly caused by left posterior cerebral artery territory infarction, the lesion disconnects the right visual cortex from the left hemisphere language centers. The left visual cortex is destroyed. The patient cannot read in the intact left visual field, but other language functions are normal. See figure 18.

Unilateral neglect

Patients fail to respond, or respond more slowly, to stimuli presented in the field opposite the lesion. They may initially appear hemianopic, or hemianesthetic, but eventually it can be shown that sensory function is normal, if their attention can be maintained. Patients may also have anosognosia: failure to recognize their deficits. They may explicitly deny a hemiplegia, or fail to recognize that they have had a stroke. Neglect is more frequent and more severe with right than with left hemisphere lesions.

The amnesic syndrome

The core features of the amnesic syndrome are: (1) Anterograde amnesia, an inability to learn new information after the onset of amnesia. (2) Retrograde

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amnesia, an inability to retrieve information that was learned prior to the onset of amnesia. (3) Normal attention and intellectual function: Many amnesics have normal language, praxis, visuospatial, and even frontal lobe function. Unless you specifically test memory, they may appear to be normal. Furthermore, certain kinds of memory are spared in the amnesic syndrome: patients can learn routines such as motor skills, and mirror reading; their behavior may be influenced by information that they cannot consciously recall. These spared functions are thus mediated by different brain structures. It is thought, for example, that motor memories and habits may be mediated through the basal ganglia, but this remains to be clarified. Diseases associated with the amnesic syndrome include stroke or tumor, if any of the critical areas is affected, head injury, Wernicke-Korsakoff disorder from thiamine deficiency, and Alzheimer's disease (which affects the hippocampus and basal forebrain). In Alzheimer's disease, cognitive deficits (aphasia, apraxia, visuospatial disorders) soon combine with amnesia to produce a more complex clinical picture.

Frontal lobe syndromes

The frontal lobes have a high-order executive role in behavior. Without their guidance, we are left at the mercy of immediate stimuli. Frontal patients may therefore demonstrate stimulus-bound behavior: they may use available objects even when there is no reason to do so (utilization behavior), they perseverate (re-use the most recent responses), and they do not seek understanding beyond what is most obvious. They may demonstrate pseudopsychopathic behavior, failing to consider the consequences of their actions, making irresponsible decisions in business, and at times making inappropriate sexual advances (despite often overall reduced libido). Patients with frontal dementias also fail to organize their experience, and do not plan for the future. They often forget things, not because they cannot encode new memories, but because they fail to initiate memory searches when appropriate. For example, the patient may be told to go to the store to buy five items, but when he gets to the store he is attracted to a magazine, reads it, and then comes home with nothing. When asked why he was sent to the store, he can recall the items he was supposed to have purchased; he just forgot to remember them when it was appropriate. [The patient with the classical amnesic syndrome would not recall the list after distraction.] Patients with orbitofrontal lesions appear to have most difficulty inhibiting inappropriate behavior. Patients with medial lesions tend to be akinetic, and fail to initiate behavior.

6.The Peripheral Nervous System, Neuromuscular Junction, and Muscle Neurological problems frequently result from lesions that spare the central nervous system, but involve nerve roots, plexuses, peripheral nerves, neuromuscular junction

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or muscle. We cannot hope to review the anatomy of all the nerves and muscles in the body, but we will summarize the deficits resulting from pathology in various peripheral sites, and will list a few nerves that you should be familiar with.

Roots, plexuses and nerves: Motor deficits

These are the features of lower motor neuron dysfunction, and include weakness, atrophy, and, at times, fasciculations (spontaneous firing of one nerve fiber, resulting in contraction of the muscles fibers that it innervates). The distribution depends upon the nerve(s) affected.

Sensory deficits

These may reflect damage to large sensory fibers (loss of vibration and position) or to small fibers (loss of pain and temperature) or both.

Autonomic deficits

Changes in skin temperature and sweating often accompany peripheral nerve lesions, but are difficult to assess reliably.

Tendon reflexes

mediated by affected nerves are diminished or absent, unless the lesion spares large sensory fibers that carry the afferent impulse from muscle spindles to the spinal cord.

Neuromuscular junction Diseases restricted to the neuromuscular junction obviously produce no sensory symptoms. The distribution of weakness depends upon the condition: myasthenia gravis has a predilection for eyelid, extraocular, bulbar and proximal limb muscles, and thus presents most commonly with ptosis, diplopia, dysarthria, dysphagia, and proximal limb weakness.

Muscle For reasons that are not clear, most primary diseases of muscle (myopathies) present with weakness that is greater proximally than distally. Myopathy should be strongly considered in patients with proximal weakness, normal sensation, and normal or depressed reflexes (severe muscle weakness or damage to the muscle spindle may depress reflexes in myopathy).

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A more detailed consideration of the distribution of findings in disorders affecting roots, plexus and peripheral nerves The diagnosis of disorders affecting the peripheral nervous system affecting the peripheral nervous system begins with localization. Although it is not possible to teach you a single set of algorithms that cover every condition, the following are basic and clinically very useful distinctions:

Median nerve

Focal neuropathies (mononeuropathy, multiple mononeuropathy)

These are isolated disturbances of single, named, peripheral nerves, such as the median or peroneal nerves. Pain can be a prominent complaint.

Mononeuropathies

Involvement of a single nerve. Trauma and nerve entrapments are the usual causes. You should be familiar with the following commonly affected nerves:

Median nerve

Often compressed as it runs through the carpal tunnel, the median nerve supplies sensation to the thumb, index, middle and half of the ring finger, and the lateral aspect of the palm. Atrophy and weakness is most obvious in the thenar muscles (abductor and opponens pollicis muscles). Carpal tunnel syndrome usually presents with pain associated with wrist flexion or extension (which narrow the carpal tunnel), and intermittent numbness. The pain may be referred to the forearm, arm, shoulder or even neck; the numbness is in the distribution of the median nerve.

Ulnar nerve

Often damaged as it wraps around the elbow, the ulnar nerve supplies sensation to the little and half of the ring finger, and the adjacent portions of the hand. Atrophy and weakness affect the interossei (most visible in the first dorsal interosseous muscle), and thumb adductor. Finger spreading and thumb adduction are weak.

Radial nerve

Usually compressed in the arm as it winds around the humerus, the radial nerve supplies sensation to the portions of the hand not innervated by median or ulnar nerves, but motor deficits predominate. There is wrist drop with weakness of finger and wrist extensors. The brachioradialis muscle is also affected. Usually the nerve is compressed after it has given off its branches to the triceps, so this muscle (and the triceps reflex) is spared.

Peroneal nerve

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The peroneal nerve is often damaged as it runs behind the head of the fibula just below the knee. Deficits include a foot drop with weakness of ankle eversion and dorsiflexion, and sensory loss along the anterolateral aspect of the leg and the dorsum of the foot.

Lateral femoral cutaneous nerve

This purely sensory nerve supplies sensation to the anterolateral aspect of the thigh. Patients complain of tingling or burning sensation in this region. The syndrome is called meralgia paresthetica. It is thought to result from entrapment or compression of the nerve as it crosses the inguinal ligament.

Multifocal neuropathy

(AKA multiple mononeuropathy, or mononeuropathy multiplex): Successive involvement of individual nerves. When the onset of symptoms in each nerve is acute and associated with pain, suspect a vasculitis (inflammation affecting the vasa nervorum).

Polyneuropathy

Polyneuropathy is the commonest generalized disorder affecting the peripheral nervous system. In polyneuropathy, usually the longest nerves are affected most severely. The initial symptoms are therefore in the feet (tingling, burning, numbness), and the earliest signs are atrophy of intrinsic foot muscles, a graded stocking distribution of sensory loss, and decreased or absent ankle stretch reflexes. As the neuropathy becomes more severe, the sensory loss ascends the legs, and then begins in the fingers. Polyneuropathies are most often caused by drugs, toxins, and metabolic diseases.

Polyradiculoneuropathies

This term is used to describe processes that can affect many portions of many nerves, resulting in both proximal and distal motor and/or sensory changes, usually with diffusely hypoactive or absent tendon reflexes. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP, commonly known as the Guillain-Barr syndrome), an autoimmune process, is the commonest example of such a neuropathy.

Plexopathy

This localization should be suspected when there are motor and reflex deficits restricted to one limb, but involving more than the territory of a single nerve or nerve root. Pain is common. Trauma, tumors, and autoimmune neuropathies may affect the brachial or lumbosacral plexus. Diabetes is a common cause of lumbosacral plexopathy.

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Radiculopathy

Radiculopathy is commonly associated with pain radiating from the neck or back to the limb. Motor, sensory and reflex deficits may be absent or slight. When present, they should be confined to the distribution of a single nerve root. Herniated disks, spondylosis, and Herpes zoster (shingles) are common causes of radiculopathy. Tumors must be considered; Lyme disease may present with polyradiculopathy. Disks, spondylosis, and tumors may also compress the spinal cord, producing combined radiculopathy and myelopathy (spinal cord dysfunction).

A note about diabetes

A note about diabetes: This is far from neuroanatomy, but this is a convenient place to mention that diabetes can cause almost any kind of neuropathy. Polyneuropathy, plexopathy, radiculopathy, mononeuropathy and multifocal neuropathy have all been ascribed to diabetes.

This creates an interesting finding on the reflex examination: when you tap the biceps tendon, the elbow extends! This occurs because (1)ðthe biceps reflex is reduced, and (2)ðthe triceps reflex is so brisk that the movement induced by tapping the biceps tendon triggers a triceps reflex. This has been called Ainversion of the biceps reflex. In addition, the finger flexor reflex can also be triggered.

It is now known that there are multiple representations of the homunculus in primary motor and sensory cortices, and there are multiple visual association areas, ecah subserving a different function (e.g., perception of color, form, or motion). This suggests that there is parallel processing of motor and sensory information. We know that spatial localization of visual stimuli is mediated by projections from occipital to parietal cortex, whereas the identification of objects by vision is mediated by projections from occipital to inferior temporal cortex. Bilateral parietal lesions can impair the patient=s ability to understand the spatial relations of objects, each of which can be identified; whereas bilateral inferotemporal lesions can impair object identification, without impairing spatial localization.

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Skill Headache history (Neurology) Tuesday, 25-9-2009

Learning outcome

Take a history from a patient who presents with a headache and differentiate between the following:

• Migraine • Tension Headache • Raised intracranial pressure • Meningism

Learning point! Headaches involve mild to severe pain in one or more parts of the head as well as the back of the neck. There are many different types of headache and these will be covered in your attachments and further studies. A few causes for headaches include:-

MIGRAINE HEADACHES: The term migraine is a corruption of the latin hemicrania or 'half the head'. Classical migraine is a headache which involves one half of the head at a time with other associated symptoms like photophobia (light insensitivity), visual upset, nausea, sleepiness and tingling. It afflicts about 2% of the population and can be dramatic in its effects, lasting from an hour to several days, causing the patient to leave work and lie down in a dark room. Common migraine affects about 10% of the population with generalised throbbing headache all over the head and drowsiness. Migraine headaches can vary in presentation and can cause a considerable impact on the daily life of sufferers. Some of the diagnostic points to migraine include:-

• Attacks can last from 4 to 72 hours • Patients are usually symptom-free between attacks • Typcailly has two of the following features:

a. Unilateral (on one side) b. Pulsating c. Moderate to severe d. Aggravated by routine activities

• Accompanying symptoms may include a. Photophobia (more sensitive to light) b. Phonophobia (more sensitive to noise) c. Nausea and Vomiting

Approximately 10 per cent of patients will have reversible sensory symptoms in the hour preceding the headache. These symptoms are known as aura and will often include visual changes, such as zigzag lines or scotoma (holes in the vision), but a variety of other symptoms may also occur. Other symptoms include, dizziness, numbness and "word salading" (words being mixed up). About 40 per cent of patients describe more vague symptoms of aura that can last substantially longer. In the day or two before an attack, prodromal symptoms, such as cravings and lethargy, can be observed. From within these two groups of symptoms, useful warnings can be identified and patients taking simple treatments during such a warning may have success in heading off a migraine before it has started. Often ignored is the postdrome phase of migraine. Once the headache has subsided the postdrome usually involves the patient feeling quite washed out or hung-over. In some patients: certain foods can trigger migraine headaches (e.g. chocolate, coffee); can occur with menses or when the patient is over tired.

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TENSION TYPE HEADACHES: Less than 2% of the population never experience the minor irritating headaches that afflicts most of us from time to time. No one knows why we suffer tension headache. They tend to come at times of stress and often result in a vicious cycle of worry and concern for the patient. Typically tension headaches are mild to moderate only, non-pulsating and bilateral. Sensory sensitivity to noise or light is more likely to be associated with migraine headaches. Difficulties arise when patients who are suffering from migraine are misdiagnosed as having tension headache. They then do not receive appropriate management. Patients often describe the pain as a 'feeling of tightness or squeezing' or a ‘tight band’ across their head. The causes of tension headache are not known. It is possible but rare to get tension headache without exacerbations - causing daily or near daily background symptoms.

MENINGISM: This is the state of abnormal irritation of the lining of the brain - the meninges. Infection by viruses, bacteria and other organisms can result in meningitis. The spinal fluid in healthy people looks clear, but when a blood vessel bursts, producing blood-stained cerebrospinal fluid, the linings of the brain are painfully irritated causing headache. The characteristics of this are - pain at the back of the neck, with resistance to passive flexion of the neck (neck stiffness) and drowsiness. The patient may find that movement aggravates and lying still may partly relive their pain.

SYMPTOMS OF RASIED PRESSURE WITHIN THE SKULL: These are particularly important to recognise. The brain in adults lies in an enclosed bony box, with a few narrow portals of entry, the principal being the foramen magnum when the spinal cord and brain are joined together. When pressure rises within the head the lowest parts of the brain, the medulla and the cerebellar tonsils are forced into the foramen magnum. This is potentially lethal. There are many causes for increased intracranial pressure including brain tumours. It is important that early symptoms of increased intracranial pressure be recognised. The cardinal feature is steadily increasing headache day by day, worse in the morning with drowsiness. The headache may be made worse by coughing, stooping or straining manoeuvres which increase the pressure within the head of normal individuals. Where the space for expansion is reduced in disease states, headache results.

There are many other types of headaches (e.g. temple arteritis, cluster headaches, referred pain from sinusitis /dental pain / TMJ dysfunction / many more…..) which will be covered later on in your course. One type of headache worth mentioning are headaches due to subarachnoid haemorrhage : A subarachnoid haemorrhage is a serious, potentially life-threatening condition. It is a very rare condition (there are less than 10,000 in the UK every year) although it is always serious and needs urgent medical attention. There are three membranes that cover the brain and spinal chord. Together they are known as the Meninges. They are: Pia mater (inner membrane), Arachnoid mater (middle membrane), and Dura mater (outer membrane). Between the inner membrane and the middle membrane is a network of blood vessels which are surrounded by a clear fluid (known as cerebrospinal fluid). In a subarachnoid haemorrhage, one of these blood vessels bursts and blood leaks out into this subarachnoid space. Typically, but not always, patients will describe their headache as the worst ever, and is usually (but again not always) of sudden onset. Neck stiffness may take hours to develop. In elderly patients particularly, classic symptoms and signs may be absent.

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Procedure

INTRODUCTION, PATIENT IDENTIFICATION & CONSENT

PRESENTING COMPLAINT “What problems brought you to the doctors today?”

HISTORY OF PRESENTING COMPLAINT Enquire about characteristics of headache:

• Site (unilateral / bilateral / neck / around eye?) • Character (Sharp / dull / ”tight band” / throbbing?) • Duration (Seconds/minutes/hours/days/weeks?) • Frequency (One off / intermittent / progressive / constant?) • Onset (Insidious/acute/gradual) • Severity (e.g. Score between 0-10; 10 = “worse headache they have ever had”) • Radiation (to other parts of the head / eye / neck) • Aggravating factors (Leaning forward /bright lights / sound / lying flat?) • Relieving factors (standing / sitting / lying still?) • Special times (Morning / menses / when overtired / stress) • Associated (Nausea / visual disturbance / drowsiness / other neuro symptoms)

Include full enquiry of all other neurological symptoms

PAST MEDICAL HISTORY Make a full enquiry about the patient’s past medical history, specifically any neurological conditions and previous headaches.

DRUG HISTORY Make a full enquiry bout any medications that a patient may be taking. Some patients may purchase mediations “over the counter” and it is important that you know about this.

FAMILY HISTORY Enquire about the patient’s family medical history. Specifically enquire if there is any history of migraine, cerebral artery aneurysms or other neurological conditions.

SOCIAL HISTORY Occupation? Has their symptoms affected their ability to work? Alcohol consumption (Units per week) Smoker? (Type / amount per day) Impact of symptoms on lifestyle

SYSTEMATIC QUESTIONING

SUMMARY OF MAIN FINDINGS TO PATIENT

PROGRESS ON TO PHYSICAL EXAMINATION.

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CHECK LIST Headache history

SKILL DETAIL CHECK

INTRODUCTION Introduce yourself & identify the patient’s details.

CONSENT Gain informed consent from the patient

PRESENTING COMPLAINT Reason for patient seeking medical advice; Onset of symptoms?

HISTORY OF PRESENTING COMPLAINT Further exploration of the presenting complaint.

-pain history

• Site (unilateral / bilateral / neck / around eye?) • Prodromal symptoms? • Character (Sharp / dull / ”tight band” / throbbing?) • Duration (Seconds/minutes/hours/days/weeks?) • Frequency (One off / intermittent / progressive / constant?) • Onset (Insidious/acute/gradual) • Severity (e.g. Score between 0-10; 10 = “worse headache ever”) • Radiation (to other parts of the head / eye / neck) • Aggravating factors (Leaning forward /bright lights / sound / lying flat?) • Relieving factors (standing / sitting / lying still?) • Special times (Morning / menses / when overtired / stress) • Associated (Vomiting / drowsiness / temp / rash etc)

• Cognitive / higher function changes? • Mood / mental state alteration? • Visual disturbances? • Speech alteration? • Episodes of loss of consciousness? • Seizures? • Sensory symptoms (numbness; pins & needles?) • Motor symptoms (involuntary movements; reduction of power?)

PAST MEDICAL HISTORY General enquire; also specific enquiry

DRUG HISTORY Any prescribed medication? Over the counter medication? Allergies?

FAMILY HISTORY General enquiry; Also targeted enquiry?

SOCIAL HISTORY Occupation / alcohol / smoking history Effect of symptoms on lifestyle / work

SYSTEMATIC QUESTIONING

SUMMARIZE TO PATIENT Allows patient to confirm that you have the right story

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Documents

SEMESTER V BLOCK 9v1.fk.ub.ac.id/id/pu/BlockIX TA 2009-2010 Student...5) Sudjari, dr. (Department of Parasitology) 6) Mudjiwiyono, dr, SpPA. (Department of Pathology Anatomy) 7) Dr