Curriculum Vitae

Resource Exchange Programmed For Asia (REP-ASIA), Singapore,

2010
Secretary of:
National Pain Study Group of Perdossi
Indonesian Pain Society
Chief of :
Pain Study Group of Perdossi Chapter Jogjakarta
Pain Sub Department, Neurology Department , Universitas
Gadjah Mada
Staff of Neurology Department, Faculty of Medicine, Universitas
Gadjah Mada

PAIN
(BASIC CONCEPT OF PAIN)

Yudiyanta
Pain Sub-Dept. of Neurology GMU

KUNJUNGAN POLIKLINIK SARAF RSS TH 2006

Defining of Pain
Pain Experience
An
xie
ty

Catastrophization

International Association for the Study of Pain

(IASP) 1994, Kyoto Protocol IASP 2008, 2011
REV

n
sio
es
pr
De

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An unpleasant sensory and

emotional experience
associated with actual or
potential tissue damage, or
described in terms of such
damage.

So
ma
ti z

ati
o

ion
t
a
ect sire
p
Ex De

&

Pain is a personal, subjective experience that comprises :

Sensory-discriminative, Motivational-affective and Cognitive-evaluative dimensions
Ronald Melzack, Textbook of Pain 4th edition

Classification of Pain

Physiologic / nociceptive:1
Pain arising from activation of nociceptors
Caused by mild and short noxious impulses which usually relieved without any
medication or mild analgesics
Example: Pinched, stung by mosquito

Inflammatory:2
Pain caused by injury to body tissues (musculoskeletal, cutaneus or visceral)
Example: Pain due to inflammation, limb pain after fracture

Neuropathic:1
Pain arising as a direct consequence of a lesion or disease affecting the somatosensory
system
Example: DPN, PHN

Psychogenic (functional):3
Pain due to abnormal responsiveness or function of the nervous system without
neurologic deficit or peripheral abnormality.
Example: Fibromyalgia, irritable bowel syndrome

Type or Category of Pain

3. Psychogenic
clear that
no somatic disorder
is present

1. NociceptiveInflamatorik
Caused by activity
in neural pathways
in response to potentially
tissue-damaging stimuli

fracture /
Postoperative
Ongoing or
impending injury

4. Mixed type
Caused by a
combination of both
primary injury or
secondary effects

2. Neuropathic
Initiated or caused by
primary lesion or
dysfunction
in the nervous sys.

sprain
Inflamation /
Infection
Muscle Stretch

strangulated
(scar tissue)
Myofascial pain

inflamed (infection )

Infiltrated or compressed
(tumors)

The Assessment of the Patient with Pain, Steven Richeimer, M.D. Director USC Pain Management, USC Medical Center, Los Angeles, CA, USA, 2007

The Continuum of Pain1

Insult
Time to resolution
Acute
Pain

<1 month

Usually obvious tissue damage

Increased nervous system activity
Pain resolves upon healing
Serves a protective function

1. Cole BE. Hosp Physician. 2002;38:23-30.

2. Turk and Okifuji. Bonicas Management of Pain. 2001.
3. Chapman and Stillman. Pain and Touch. 1996.

Chronic
Pain

3-6 months

Pain for 3-6 months or more2

Pain beyond expected period
of healing2

Usually has no protective

function3

Degrades health and function3

Small-fiber sensory
-Burning pain
-Allodinia
-Hyperalgesia
-Hyperesthesia
-Paresthesia/dysesthesia
-Lancinating pain
-Loss of pain & temp.
sensation
-Foot ulceration
-Loss of visceral pain

Large-fiber sensory
-Loss of vibration
-Loss of proprioception
-Loss of reflexes
-Slowed NCV

Autonomic
-Heart rate abnormalities
-Postural hypotension
-Abnormal sweating
-Gastroparesis
-Neuropathic diarrhea
-Impotence
-Retrograde ejaculation

Normal Nerve Impulses Leading to Pain

Perceived pain

Noxious
stimuli
Descending
modulation

Ascending
input

Nociceptive afferent fiber

Spinal cord

Perception

Nociception

Pain

Modulation
Descending
modulation
Ascending
input

Dorsal Horn
Dorsal root
ganglion

Transmission
Transduction

Spinothalamic
tract

Peripheral
nerve

Peripheral
nociceptors

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.

Trauma

Transduction

KERUSAKAN JARINGAN
INFLAMASI
SENSITISASI
SSA

Si-Na+

MI

AKTIFASI
Pg
B, 5HT, Adenosin

ECT. DISC.
R-NE

Activation

NOS

KORNU DORSALIS

Pengalaman
Kognitif
Behaviour
Psikologik

Inhibisi
desenden

OTAK
PAIN NO PAIN

External Heat

VR1
Ca

Mechanical

Stimuli

Pain and auto-sensitization

2+

Na+

mDEG ACTION
ACTION POTENTIAL
POTENTIAL
Voltage gated sodium channels
P2X3

ATP
Chemical

Generator potentials

action potentials
Woolf & Mitchel, 2001
Modifikasi Meliala, 2003

Anger

Anxiety

Fear

Depression
PSYCHOLOGICAL

NOCICEPTIVE

Noxious Stimuli

MELIALA 2004

What is Inflammatory Pain?

Often classed along with acute pain as nociceptive, refers to the
spontaneous pain and tenderness felt when tissue is inflamed.
Pain caused by injury to body tissues (musculoskeletal, cutaneous or
visceral)
Painful region is typically localized at the site of injury often described as
throbbing, aching or stiffness .
Usually time-limited and resolves when damaged tissue heals (e.g. bone
fractures, burns and bruises)
Can also be chronic (e.g. osteoarthritis, rheumatoid arthritis)
Usually responsive to NSAIDs

NOCICEPTIVE PAIN

Inflammation Tissue
1

Prostaglandins produced
in response to tissue
injury; increase sensitivity
of nociceptor (pain)

Nociceptor then releases

substance P, which dilates
blood vessels and increases
release of inflammatory
mediators, such as Bradykinin
(redness & heat)

Substance P also promotes

degranulation of mast cells,
which release histamine
(swelling)

Painful stimulus

Pain-sensitive tissue

Prostaglandin

Mast cell

Substance P

Blood
vessel

Histamine
Bradykinin
Substance P

3
Nociceptor

What is Neuropathic pain?

Definition:
Pain arising as a direct consequence of a lesion or disease affecting
the somatosensory NERVE system

Characterized by:
Pain often described as shooting, electric shock-like or burning.
The painful region may not necessarily be the same as the site of
injury.
Almost always a chronic condition (e.g. post herpetic neuralgia, post
stroke pain)
Responds poorly to conventional analgesics

IASP Classifications:
Peripheral Neuropathic and Central Neuropathic Pain
Neuropathic pain
Pain arising as a direct consequence of
a lesion or disease affecting the
somatosensory system

Peripheral neuropathic pain

Central neuropathic pain

Pain arising as a direct consequence of

a lesion or disease affecting the
peripheral somatosensory system

Pain arising as a direct consequence of

a lesion or disease affecting the
central somatosensory system

Loeser JD, Treede RD. The Kyoto Protocol of IASP Basic Pain Terminology. Pain 2008;137:473-477.

Pathophysiology of Neuropathic Pain

Peripheral mechanisms
Peripheral Neuron
hyperexcitability

Central mechanisms
Loss of
inhibitory controls

Central Neuron
hyperexcitability
(central sensitization)

Abnormal
Discharges

NeP

Peripheral Mechanism (Ectopic Discharges)

Nerve lesion induces hyperactivity due to changes in ion channel function

Perceived pain

Nerve lesion
Descending
modulation

Ascending
input

Nociceptive afferent fiber

Spinal cord
Ectopic discharges

Central Mechanism (Loss of inhibitory controls)

Loss of descending modulation causes exaggerated pain due to an imbalance
between ascending and descending signals
Exaggerated pain
perception

Noxious
stimuli

Loss of
descending
modulation

Ascending
input

Nociceptive afferent fiber

Spinal cord

Central Mechanism (Central sensitization)

After nerve injury, increased input to the dorsal horn can induce central
sensitization
Perceived pain
Nerve lesion
Descending
modulation

Ascending
input

Nociceptive afferent fiber

Perceived pain
(allodynia)

Abnormal discharges induce central sensitization

Tactile
stimuli

Descending
modulation

Intact tactile fiber

Ascending
input

Development of Neuropathic Pain

Etiology

Pathophysiology

Nerve damage due to:

Metabolic

Traumatic

Ischemic

Toxic

Hereditary

Infectious

Compression

Immune-related

Mechanisms

Symptoms

Spontaneous pain Stimulus-evoked pain

Syndrome

Neuropathic pain

Woolf and Mannion. Lancet 1999;353:1959-64

Signs and Symptoms of Neuropathic Pain

Sign/Symptom

Description (example)

Spontaneous symptoms
Spontaneous pain1

Persistent burning, intermittent shock-like or

lancinating pain

Dysesthesias2

Abnormal unpleasant sensations

e.g. shooting, lancinating, burning

Parasthesias2

Abnormal, not unpleasant sensations e.g. tingling

Stimulus-evoked
symptoms
Allodynia3

Pain due to a stimulus that does not normally

provoke pain. e.g. warmth, pressure, stroking

Hyperalgesia3

Increased pain from a stimulus that normally

provokes pain. e.g. pinprick, cold, heat

Hyperpathia2

Delayed, explosive response to any painful stimulus

1. Baron. Clin J Pain. 2000;16:S12-S20.

2. Merskey H et al. (Eds) In: Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 1994:209-212.
3. Loeser JD, Treede RD. The Kyoto Protocol of IASP Basic Pain Terminology. Pain 2008;137:473-477

Hyperalgesia & Allodynia

10

Pain Intensity

Hyperalgesia

6
Allodynia

Normal
Pain
Response
Injury
Hyperalgesiaheightened
sense of pain to noxious
stimuli

Allodyniapain resulting
from normally painless
stimuli

2
0
Stimulus Intensity
Gottschalk A et al. Am Fam Physician. 2001;63:1979-84.

The Inter-Relationship Between

Pain, Sleep, and Anxiety / Depression
Pain

Functional
impairment
Anxiety &
Depression

Nicholson and Verma. Pain Med. 2004;5 (suppl. 1):S9-S27

Sleep
disturbances

What is the Correlation Between Causes, Muscular pain,

Neuro-endocrine (HPA Axis) disorders and Psychological distress
Emotional, Environmental and Genetic Predisposition
Cortex-Limbic System- Hypocampus

Perception

Thalamus & Hypothalamus

CRH, TRH, GhRH, PRF, GnRH

Pituitary

ACTH, TSH, GH, Prolactine, FCH-LH

Adrenal,
Thyroid

Cortisone,
Thyroid,
Prolactine, Estrogen, Progesterone

Neuro-hormonal Disfunction
Sympathetic

Metabolic

Dorsal Horn

Muscle Trauma

PAIN

PAIN ASSESSMENT

The 3L Approach to Diagnosis

LISTEN
Patient verbal descriptors,
Q&A

LOCATE

LOOK

Nervous system
lesion / dysfunction

Sensory abnormalities,
pattern recognition

Pain Assessment Scales

Uni-Dimensional Scale
Only measures pain intensity
Appropriate for acute pain
The most common scale used in
outcome assessment (Analgesic
efficacy)

Verbal Rating Scale (VRS)

None, mild, moderate, severe
Numeric Rating Scale (NRS)
Visual Analog Scale (VAS)
Pictorial Scale

Multi-Dimensional Scale
Both intensity (severity) and
unpleasantness (affective)
Appropriate for chronic pain
Research /pathophysiology
Should be used in clinical
outcome assessment

McGill Pain Questionnaire (MPQ)

The Brief Pain Inventory (BPI)
The Memorial Pain Assessment Card

Uni-Dimensional Pain Assessment Scales

Photographic/Numeric Pain Scale

Multi-Dimensional Pain Assessment Scales

Treatment

Relief

General Activity
Mood
Walking ability

Worst

Normal work

Least

Relation with other people

Sleep

Average
Enjoyment of life
Right Now

Quicker and easier

Well established reliability
in cancer, arthritis, and
AIDs.
Sensory, affective and
functional status
Useful for treatment
response
Takes up to 15 min
Good choice for patients
with progressive disease

Patient Pain Diary

Pain Scale

10

Dose
Morning

Dose
Afternoon

Evening

Bedtime

ID PAIN : Screening tool to help differentiate

nociceptive from neuropathic pain
Neuropathic pain screening questionnaire
A multicenter study
Patients (N = 586) with non-headache chronic pain A second
multicenter study (N = 384) evaluated reliability and validity.
89-item questionnaire 6 items
ID Pain appeared to accurately indicate the presence of a
neuropathic component of pain (c 74,2%)
Portenoy R et al. Curr Med Res Opin. 2006 Aug;22(8):1555-65.

Location: Patient or nurse marks drawing

Intensity: Patient rates the pain. Scale Used:

Quality: Use patints words, e.g. prick, ache, burn, sharp, hot etc.
Onset, duration, variations, rhythms (spontaneus or evoked):
Manner of expressing pain: (Pain Behaviour)
What relieves the pain?

What causes or increases the pain?

Effect of pain: (Note decreased function, decreased quality of life)
Accompanying symptoms (eg nausea)
Sleep
Appetite
Physical activity
Relation with others (eg irritability)
Emotion (eg anger, suicidal, crying)
Consentration
Other

Other comments:
Plan:

Past Medical History

1. Medical related problems
2. Problems potentially affect the choice of pain
treatments?
3. Prior or current substance abuse history?

Current Medications
1. Dosage and pattern of use
2. Effectiveness
3. Drug tolerance

Physical Examination

The history will often generate a differential diagnosis

The physical exam will often lead to the selection of the primary
diagnosis, and occasionally a test will help to confirm this diagnosis

1.
2.
3.
4.

Mental status exam (facial expression)

Vital signs
Inspection (body position, gait, redness, swelling)
Palpation & Musculoskeletal exam (atrophy, location
tenderness to pressure, mass, )
Neurologic Examination (Sensory, Motor, Autonomic)

5.

NEUROLOGIC EXAMINATION
Possibility :
spinal cord compression,
nerve root lesions
peripheral nerve lesions

Sensory Exam.:
numbness,
allodinia,
hyperalgesia

Motoric: fracture?
Deep tendon reflexes
Sacral Reflexes

Psychological Evaluation
1.
2.
3.
4.
5.
6.
7.
8.

Mood disorder (50% chronic pain)

Somatization
Secondary gain
Sleep and appetite disturbance
Loss of energy and libido
Impaired concentration
Suicidal ideation
Impact of the pain on the patient

day-to-day activities
work & finances
personal relationships
recreational pursuits

CONCLUSIONS

You are the only one who knows how much pain you are feeling
All patients require pain assessment
it is as essential as the other vital signs!
(Helen Greene)

If You Dont Measure It, You Cant Improve It

(Field et al, 1997)