PAIN PATHOPHYSIOLOGY AND

ASSESSMENT
DR PRADEEP KULKARNI
 Pain is
• The most common symptoms in patients with
cancer
• and it is certainly the most feared.

“Pain is what the patient says, hurts.”

Believe the patient

about his/her pain!
 Incidence
• Pain and advanced cancer are not synonymous.
- ¾ of patients experience pain.
- ¼ of patients do not experience pain
• Most cancer patients have more than one type
of pain(80%)
 IASP definition of pain

Pain is an unpleasant , sensory and

emotional experience associated with
actual or potential tissue damage or
described in terms of such damage.
(International Association for the study of
pain,1979)
Concept of ‘Total Pain’
Emotional
Physical Anger
Symptom Disfigurement
Treatment effects Fear of death
Fatigue Feeling of helplessness
insomnia
Total
pain
Social Spiritual
Family worries Why me?
Loss of income Meaning?
Loss of social role Punishment?
isolation Purpose in life?

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 Neuroanatomy of pain
The parts of the nervous system responsible for
the sensation and perception of pain may be
divided into three areas:

1) Afferent pathways

2) CNS

3) Efferent pathways
 Pain
Specialized receptors = Free nerve endings
Stimuli (Tissue Damage)
◦ Mechanical Damage
◦ Extreme Temperature
◦ Chemical Irritation
Two Types of Neurons
◦ A – Delta fibers for sharp pain
◦ C – Fibers for dull pain
Four Distinct Processes
◦ Transduction, Transmission, Modulation, Perception

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 Afferent Pathway
Nociceptors

A delta fibres C fibres

(Well localised sharp pain) (Diffuse burning aching pain)

Spinal cord Dorsal Horn

Spinothalamic tract
Pain Pathway

SIMPATICO PALLIATIVE CONNECT, PUNE 9

 Classic pain pathway A delta
Nociceptor – inflammatory soup
Diameter, speed and myelin
Dendrite and axon
DRG
Pre synaptic and post synaptic
Decussation
Thalamus
Sensory Homunculus
Sharp, localised pain
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 Classic pain pathway C fiber
• Diameter, speed, no myelination
• Decussation
• Medial to STT
• Below the thalamus ramifications
• Limbic system- emotional component
• Reticular- sleep disturbances
• Dull aching, diffuse, emotional component

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 Dual Nature of Pain : Fast and Slow
• Fast Pain • Slow Pain
– Acute – Chronic
– Pricking Type – Throbbing Type
– Well Localized – Poorly Localized
– Short Duration – Long Duration
– Involving A Delta – Involving
Fibers Unmyelinated C
– Fast Conduction 20 Fibers
m/s – Slow Conduction 1 –
– Somatic Pain 2 m/s
– Visceral Pain
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Ascending analgesic pathway- Analgesia

• Gate theory
• TENS
• Massage
• Rubbing
• Hot or cold fomentation

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 Descending analgesic pathway
• When survival is at stake
• Brain
• Hypothalamus
• Periaquiductal gray matter
• Nucleus of Raphe
• Dorsal horn
• NE, 5HT3, Endorphins, GABA

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 Modulations
Dorsal horn
Descending pathways
Serotonin uptake inhibitors
Norepinephrine uptake inhibitors
Morphine
Gabapentinoids
NMDA receptor antagonists
Higher centers- anxiety, expectation, placebo,
arousal, attentional/diversional
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 Pain terminologies
• Nociceptive pain- Nociceptor
• Neuropathic pain
• Analgesia- algos is pain
• Hyperalgesia
• Allodynia
• Modulation
• Referred pain
• Pain tolerance and threshold- pain when it hurts
• Sensitization – central and peripheral
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 Components of pain
• Sensory- intensity, recurrence
• Affective – anxiety, depression, insomnia
• Autonomic – tachycardia, sweating, raised
blood pressure
• Motor- withdrawal, agony, reduced, vocal

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 Aetiology of pain in palliative care
• Disease related- soft tissue infiltration, nerve
compression, bone spread, muscle spasm,
lymphoedema, raised ICT.
• Comorbidities related-Low back ache, arthritis,
angina, trauma
• Treatment related- surgery, chemo, radiation
• Debility related –pressure sore, constipation, bladder
spasm

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 Peripheral sensitization
• At sites of injury or cancer, pain occurs due to
the stimulation of the sensory nerve ending
(nociceptor).
• One of the mediators, prostaglandin, makes the
nerve-ending more sensitive to other pain-
producing substances.
• Therefore blocking the generation of
prostaglandins with NSAIDS can prevent pain
caused by the other chemicals too.
Central sensitisation “wind-up”
NMDA

The nervous system becomes more sensitive

in perceiving pain to a given stimulus.

Woolf CJ, Anesth Analg. 1993;77:362-379.

 Recruitment

Peripheral

Peripheral recruitment :
The silent or sleepy nociceptors get recruited.
Central recruitment :
Newer areas in the central nervous system get recruited so that
more areas start responding to a painful stimulus.
 Reflex responses
• Continues pain causes more and more pain by
several ways:
– Muscles go into spasm generating new pain
– Reflex vasoconstriction causes liberation of
more chemicals.
– In ischaemic pain, analgesics alone may improve
vascularity to a point

Vasoconstriction

Skeletal muscle spasm

 Worsening pain in intensity and extent

• Sensitisation of nociceptors.
• Sensitisation of dorsal horn cell.
• Recruitment of silent (sleepy) nociceptors.
• Recruitment of adjacent spinal segments
• Skeletal muscle spasm
• Vasoconstriction
 Clinical relevance?
• The earlier the pain is treated,the less these
perpetuating changes.
• All continuous pain warrant continuous
analgesia.
• Total relief is difficult if permanent changes
have taken place.
 Pain descriptions
• Acute/chronic

• superficial/deep

• Visceral/somatic

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 Pain descriptions
Acute Chronic
• Indicates tissue damage- • Multifactorial-
actual/potential neurochemical
• Autonomic responses are • Vegetative responses are
dominant dominant
• Self limiting • Unremiting, progressive
• Intensity reduces as healing • Constant reminder of life
progresses threatening disease
• Acute pain is protective; it’s • Chronic pain takes
a symptom characteristic of disease

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 Pain descriptions
Superficial Deep

• Skin, joint, muscle • Organ related

• Nociceptive • mixed

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 Types of pain

Nociceptive Neuropathic
 Nociceptive & Neuropathic Pain
• Any pain caused primarily by stimulation of
the nociceptor can be said to be nociceptive
pain.
• If pain is caused by any abnormal impulse
generated within the pathway proximal to the
nociceptor,it is called neuropathic pain.
 Nociceptive Pain
Visceral Somatic
• Capsular- visceral • Bone –cortical bone,
membrane, trabecular bone,
stretching periosteum

• Bowel – spasm, • Soft tissue

colicky

• Cardiac -ischaemia
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 Neuropathic

Nerve compression Nerve injury

Peripheral Central Sympathetically

maintained
 Neuropathic Pain Manifestations

• Nature of pain (burning, pricking, aching,

shooting, lancinating)
• Neural / dermatomal distribution
• Abnormal sensations like allodynia
 Allodynia& Hyperalgesia

• Allodynia is Pain caused by a stimulus

that normally does not provoke pain
• Hyperalgesia is increased response to a
normally painful stimulus
 Pain perception
Pain Experience and Behaviors

•Past experience,
•development, Neuronal
•Cultural factors, Pain and genetic
•Emotion Generating changes
•environment Mechanism

Somatosensory Input
Melzack, Trends Neurosci 1990; 13:88-92
 Somatisation

• When negative emotions are expressed

through physical symptoms
• Somatisation is NOT the patient’s fault!
 Conclusion
• Pain is what patient says
• Not related to tissue damage
• Emotional component
• Total pain concept
• Different types of pain require different
treatment plans

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 Why pain assessment
To capture the experience in standard way

Assess the cause, type, intensity

Effect on daily livings, relations, social

effects
Plan for rational treatment

Modify the treatment after reassessment

Help to communicate with team

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 General principles
• Settings, develop rapport, eye contact, open
ended questions
• What patient says is pain
• Tools ideal and individualized
• Family involvement may be necessary

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 When to assess pain?
• At the time of admission
• 30 minutes after giving analgesics
• Every shift
• Any time new pain appears
• As fifth vital parameter
• Family meeting, if not relieved

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 Barriers for assessment

• Lack of self reporting-child, elder, cognition

• Good patient

• Fear of drugs/procedures

• Lack of skills for doctor

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 Myths

Minor illness less pain

Increase damage more pain

Psychological pain is not real

Drug dependency

Doctor knows more

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 HISTORY
• O - when, how long, how often
• P - provocation/palliative factors
• Q - how he describes
• R - region/radiation
• S - severity
• T - temporal factors
• U - beliefs
• V - goals of care
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 Physical exam
• General exam-posture, routine exam

• Local exam-swelling, tenderness, guarding

• Nervous system- sensory system, motor

system, co ordination, sympathetic, cognition

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 Possible cause

• Acute/chronic

• Nociceptive- somatic/visceral

• Neuropathic- central/peripheral

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Pain Assessment Scales

SIMPATICO PALLIATIVE CONNECT, PUNE 45