PAIN

MECHANISMS, CLASSIFICATION AND ASSESMENT

DEPARTEMEN NEUROLOGI
FAKUTAS KEDOKTERAN
UNIVERSITAS ISLAM SUMATERA UTARA
 Pain Definition (IASP)

Unpleasant sensory and emotional

experience associated with actual or
potential tissue damage, or describe in
terms of such damage.
l

International for the Study of Pain: Pain Definition.

Bonica JJ. The need of a taxonomy. Pain 1979;6(3):247-8.
 What is Pain ?
Accepted definition:
 An unpleasant sensory (noxious) and
emotional experience associated with actual or
potential tissue damage
 Anything which would cause more than
momentary pain in humans, should be
assumed to cause pain in an animal
• Implies emotional component.
• Pain can exist without tissue
damage.
 Definition of Pain
• Pain is whatever the experiencing person says it is, existing
whenever the experiencing person says it does. McCaffery M.
(1968)
 Definitions

• Agology – the science and study of pain

• Allodynia – pain caused by a stimulus that is not normally painful
• Analgesia – the absence, or decrease, of pain in the presence of a
stimulus that would normally be painful
• Hyperalgesia – an increased sensitivity to a stimulus that is
normally painful
• Nociception – the reception, conduction, and central nervous
processing of nerve signals resulting in the perception of pain
• Somatic pain – pain originating from skin, joints, muscles, and
other deep tissues
• Visceral pain – pain originating from the internal organs
 Definitions
 Noxious stimulus – a stimulus which is actually or potentially
damaging to body tissues
 Pain threshold – the point at which an individual just begins to
feel pain; is relatively consistent among normal individuals
 Pain tolerance – the greatest amount of pain that a subject will
tolerate; varies greatly among individuals
 Radiculalgia – pain along the distribution of one or more sensory
nerve roots
 Radiculitis – an inflammation of one or more nerve roots
 Wind-up – a cascade of events resulting from ongoing stimulation
of nociceptors and activation of NMDA receptors; causes
hyperalgesia and opioid tolerance
 Types of Pain
Physiological Pain Pathological Pain
• Is a protective  Results from tissue injury
 Inflammation occurs in the
mechanism area
• Causes avoidance  Nerve damage
 Release of
• Little to no tissue neurotransmitters with
injury ongoing stimulation of
nociceptors
• Pain stops once the  Can lead to hyperalgesia
stimulus is removed  Persists after the stimulus is
removed
 Types of Pain
Acute Pain
• Occurs immediately after
a stimulus is received
• Severity can vary
• Responds well to
treatment
• Subsides once stimulus is
removed
Chronic Pain
 Persists well past initial
stimulus (3-6 months)
 Severity can vary
 May or may not respond well to
treatment; may require a
“multi-modal” approach
 Can result in allodynia,
hyperalgesia, and opioid
tolerance
 Acute Pain
• Nociceptive pain (the action of a peripheral nerve which
receives & conveys painful stimuli to the brain)

• Derived directly from pain receptors

• Arises in damaged tissues
• Sensed in damaged area
• Has a cause which is of finite duration
• Has a ‘purpose’
 Physiology of Pain Perception

 Transduction Injury Brain

 Transmission
 Modulation
 Perception
 Interpretation Descending
Pathway
 Behavior
Dorsal
Peripheral Root
Nerve Ganglion

Ascending
Pathways
C-Fiber

A-beta Fiber Dorsal

Horn
A-delta Fiber
Spinal Cord
11 Adapted with permission from WebMD Scientific American® Medicine.
 Physiology of Pain
• Damaged cells release • A-delta nociceptors are
substances which myelinated, conduct
stimulate nociceptors impulses rapidly, trigger
and inflammation sensation of first pain
(sharp, pricking pain)
• Noxious stimuli • C-fibers are
activate nociceptors, unmyelinated,
which become stimulated by chemicals
sensitized with released in damaged or
stimulation, resulting inflamed tissues, and
in a lowered mediates slow, burning
stimulation threshold pain
 Physiology of Pain
• Sensitized nociceptors • Afferent neurons in
cause the release of the spinal cord relay
glutamate and the signal to multiple
neurokinins from the areas in the brain,
afferent terminals in resulting in the
the spinal cord perception of pain
• Activates NMDA (N- • “Gate control” occurs
methyl-D-asparate) in the spinal cord,
receptors, which are resulting in early
implicated in inhibition of
hypersensitivity (wind- nociception, allowing
up) escape
 Physiology of Pain
• Stimulation of medulary • Various neurotransmitters
centers result in are released: glutamate,
hyperventilation, norepinephrine, serotonin,
increased cardiac output, gamma-aminobutyric acid
and increased blood (GABA) and endorphins
pressure • Analgesia can be induced by
• Descending neurons act blocking the nociceptive
to modulate pain by process at one or more
reducing sensation points
 Tissue Trauma

Cell Membrane Phospholipids

Phospholipase

Arachidonic Acid

C
O Cyclo-oxygenase
X

Endoperoxides

Thromboxane Toxic Oxygen Radicals

Prostaglandins Prostacyclin
 Physiology of Pain

Pain ≠ Nociception
What is the difference?
Pain is a product of higher brain center processing of
signals it has received.
Nociception refers to the peripheral and central
nervous systems processing information generated by
stimulation of nociceptors by noxious stimuli
Nociception can occur in the absence of pain.
 Physiology of Pain
There are four distinct processes involved in nociception
which can be modulated by analgesics:
– Transduction – translation of the noxious stimulus
into electrical activity at the peripheral nociceptor
– Transmission – the propagation of nerve impulses
through the nervous system
– Modulation – modification of nociceptive
transmission by inhibition of the spinal dorsal horn
cells by endorphins
– Perception – the final conscious subjective and
emotional experience of pain
Pain Pathways
Peripheral origins of pain. Noxious signaling may result from either
abnormal firing patterns due to damage or disease in the peripheral nerves or stimulation
of nociceptors (free nerve endings due to tissue trauma). Inflammation in injured or
diseased tissue sensitizes nociceptors, lowering their firing thresholds. Some clinical pain
states have no peripheral origin, arising from disorders of brain function.
Multiple pathways of nociceptive transmission for the spinal cord to central
structures. There are four major pathways the A: spinoreticular;
B: spinothalamic; C: spinomesencephalic; and D: spinohypothalamic tracts.
 Major Categories of Pain
Classified by inferred pathophysiology:

1. Nociceptive pain (stimuli from

somatic and visceral structures)
2. Neuropathic pain (stimuli abnormally
processed by the nervous system)
 Acute vs Chronic Pain

Characteristic Acute Pain Chronic Pain

Cause Generally known Often unknown

Duration of pain Short, Persists after healing,

well-characterized 3 months

Treatment Resolution of Underlying cause and

approach underlying cause, pain disorder; outcome
usually self-limited is often pain control,
not cure
 Domains of Chronic Pain

Quality of Life Psychological Morbidity

Physical functioning Depression
Ability to perform activities Anxiety, anger
of daily living Sleep disturbances
Work Loss of self-esteem
Recreation

Social Consequences Socioeconomic

 Marital/family Consequences
relations  Healthcare costs
 Intimacy/sexual activity  Disability
 Social isolation  Lost workdays
 Nociceptive vs Neuropathic Pain

Nociceptive Mixed Type Neuropathic

Caused by a Pain
Pain combination of both
Caused by activity in neural Initiated or caused by
primary injury and
pathways in response to primary lesion or
secondary effects
potentially tissue-damaging dysfunction in the nervous
stimuli system

CRPS*

Postherpetic
Postoperative
Arthritis neuralgia Trigeminal
pain
neuralgia
Sickle cell
crisis Neuropathic
Mechanical
low back pain Central post-
low back pain
Sports/exercise stroke pain
Distal
injuries
polyneuropathy
*Complex regional pain syndrome (eg, diabetic, HIV)
NOCICEPTIVE PAIN

“I’ll want to get a few tests on you, just to cover my ass”

Pain Pathway
 Why assess pain ?

• To establish degree and nature of pain

• To ensure patient comfort
• To evaluate effectiveness of analgesia
• To help alleviate anxiety
• To decide on type of analgesia
• To aid recovery and prevent complications
 Why all the fuss?

• Pain is a miserable experience

• Pain increases sympathetic output
– Increases myocardial oxygen demand
– Increases BP, HR
• Pain limits mobility
– Increases risk for DVT/PE
– Increases risk for pneumonia, atelectasis
secondary to splinting
 How to assess pain
• Communication with patient is essential
• Observe for changes in physiological signs
• Use a pain scoring system

• Body language?
• Consider pain as 5th vital sign
 Physical Exam

• Overall impression/appearance
• Facial expression
• Body position and movement
• Areas of redness, swelling, warmth
• Palpation, tenderness
• Focused assessment:
 eg. chest pain
 Pain Assessment

• No one tool is suitable for all situations

• Pain is complex with many variables, apart
from the physical cause, that can influence
the patient’s experience and interpretation
 Pain Assessment

“One of the most important functions of the nurse

is to alleviate the suffering of people who are
experiencing pain”
Schofield P(1995)
 Pain Assessment Scales
The National Initiative on Pain Control™ (NIPC™) has
provided these diagnostic tools to assist you in assessing
the severity and quality of pain experienced by your
patients..
 Where is Your Pain?
Please mark, on the drawings below, the areas where you feel pain. Write “E” if external
or “I” if internal near the areas which you mark. Write “EI” if both external and internal.
0–10 Numeric Pain Rating Scale

0 1 2 3 4 5 6 7 8 9 10

Nopain Moderate pain Worst

possible
pain
 Wong-Baker FACES Pain Rating Scale

No Hurt Hurts Little Bit Hurts Little More Hurts Even More Hurts Whole Lot Hurts Worst

Rating scale is recommended for persons age 3 years and older.

Brief word instructions: Point to each face using the words to describe the pain
intensity. Ask the child to choose face that best describes own pain and record the
appropriate number.
 FIVE QUESTION APPROACH

1. Fiber type
2. Pattern of distribution

5. Pathology

3. Temporal course

4. Key features
 1.What is the fiber type involved?
(motor, large sensory, small sensory, autonomic,
combination)
 2. What is the pattern of distribution?
(distal or proximal, symmetric or asymmetric)
 3. What is the temporal course?
(acute, chronic, progressive, stepwise, relapsing remitting)
 4. Are there any key features pointing to a specific etiology?
(toxic/nutritional/malignancy)
 5. What is the pathology?
(axonal, demyelinating)
 Good pain management
• Communication
• Tailored to individual
• Holistic
• Multidisciplinary Documentation
• Continuity
• Education of staff, patients,
relatives and visitors
 Management of acute pain
Analgesic drugs are used to treat
acute pain, the choice of drug
dependent on the intensity of pain
being experienced.
 Acute Pain Management Modalities

• Cyclo-oxygenase inhibitors
– Non-specific COX inhibitors(classical NSAIDs)
– Selective COX-2 inhibitors, the “coxibs”
– Acetaminophen is probably COX-3

• Opioids

• Local Anesthetics

• NMDA antagonists
– Ketamine, dextromethorphan
Analgesic Ladder
 Golden Rules

• By the clock

• By the ladder

• By the mouth
 Methods of administration
• Epidural Analgesia
• Patient Controlled Analgesia [ intra - venous ]
• Intra Muscular Injection
• Sub Cutaneous
• Oral
• Rectal [ suppositories ]
• Transdermal
• Inhalation [ gas ]
• Regional Nerve Blocks e.g. Paravertebral Brachial Plexus
• Wound Infiltration
• Reflexology
• Reassurance
47
48