PAIN

By Dr AravindDr Srinivas

Under Guidance ofDr DSVL Narasimham MSDr R Hemanthi MSDr P S Sitaram MS

What is pain?

• Pain from poena ---> Latin means punishment.

• There is an International definition of pain formulated by the IASP (International Association for the study of pain

• Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

IASP – International Association for the Study of Pain 2011

• It is a symptom

• Pain is ▫ Subjective

▫ Protective

▫ and it is modified by developmental, behavioral, personality and cultural factors

• Associated signs Crying

Sweating,

Increased heart rate

Blood pressure

Behavioral changes

Dual nature of pain

Fast Pain Slow pain

▫ acute

▫ pricking type

▫ well localized

▫ short duration

▫ Thin myelinatednerve fibers are involved (A delta)

▫ chronic

▫ throbbing type

▫ poorly localised

▫ long duration

▫ Unmyelinated nerve fibres are involved (c fibres)

Pain terminology• Hyperalgesia

▫ Increased pain from a stimulus that normally provokes pain• Hyperaesthesia

▫ Increased sensitivity to stimulation, excluding the special senses (increased cutaneous sensibility to thermal sensation without pain )

• Paraesthesia▫ An abnormal sensation, whether spontaneous or evoked

• Anaesthesia▫ A loss of sensation resulting from pharmacologic depression of nerve

function or from neurological dysfunction• Neuralgia

▫ Pain in the distribution of a nerve or nerves• Analgesia

▫ Absence of pain in response to a normally painful stimulus• Allodynia

▫ Pain due to a stimulus that does not normally provoke pain

• Neuropathic Pain ▫ Pain caused by a lesion or disease of the somatosensory nervous

system• Nociceptive pain

▫ Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

• Visceral pain ▫ Pain arising from visceral organs (e.g., heart, lungs, gastrointestinal

tract, liver, gallbladder, kidneys, bladder).• Neuropathy

▫ A disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy

• Nociception▫ The neural process of encoding noxious stimuli

• Noxious stimulus

▫ A stimulus that is damaging or threatens damage to normal tissues.

Different situations

• No stimuli, but pain is felt

phantom limb pain

eg. in amputated limb

• Stimuli present, but no pain felt

eg. soldier in battle field, sportsman in arena

• Pain due to a stimulus that does not normally provoke pain

• Pain caused by a lesion or disease of the somatosensory nervous system

• Pain as a sensation▫ physiologically (nociception)

▫ Nociceptive pain

• Pain as an emotional experience▫ Psychologically

▫ Psychogenic pain

• Pain caused by damage to nerve▫ Neuropathic pain

• Transduction▫ Process of converting noxious stimulus to action

potentials

• Perception▫ Central processing of nociceptive impulses in order to

interpret pain

Stimuli • Physical

▫ pressure etc

• Electrical

• Thermal▫ cold, hot

• Chemical▫ H+, lactic acid, K+, histamine, bradykinin, serotonin, leucotrines,

acetylcholine, proteolytic enzymes, capsiacin

▫ Prostaglandins (PGE2)

Cannot directly stimulate nociceptors

Increase the sensitivity of nociceptors for other stimuli (decrease the threshold)

Pain receptors are called nociceptors A sensory receptor that is capable of transducing and

encoding noxious stimuli (actually or potentially tissue damaging stimuli)

Nociceptors are free nerve endings

Free nerve endings are distributed everywhere both somatic and visceral tissues except brain tissue and lung parenchyma

• Different types of nociceptors▫ Some respond to one stimulus▫ Some respond to many stimuli (polymodal)▫ Some may not respond to the standard stimuli (silent

nociceptors) They respond only when inflammatory substances are present

• Capsaicin receptor (TRPV1 receptor)▫ Respond to capsaicin, heat, low pH▫ Stimulation leads to painful, burning sensation

Nerve pathways• Afferent fibers• Two types▫ A (thin myelinated)▫ C (unmyelinated)

• Pain signals enter the spinal cord

• First synapse is present in the dorsal horn of the spinal cord

• Then the second order neuron travels through the lateral spinothalamic tracts

• First synapse in spinal cord is substantia gelatinosa

substantia

gelatinosa

Neurotransmitter at the first synapse of the

pain pathway is substance P

• Acute pain : glutamate

• Chronic pain: substance P

• Pain inhibitory neurotransmitters: enkephalin, GABA

• Ascending pathway Crosses the midline

Ascends up as the lateral spinothalamic tract

Pain

lateralspinothalamic tract

C fibre

substantiagelatinosa

lateralspinothalamic tract

thalamus

C fibre

thalamocorticaltracts

Pain perception• Thalamus is an important centre of pain perception▫ Lesions of thalamus produces severe type of pain

known as ‘thalamic pain’

• Sensory cortex is necessary for the localisation of pain

• Other areas are also important▫ Reticular formation, limbic areas, hypothalamus and

other subcortical areas

Descending pain modulatory system

• Stimulus produced analgesia (Reynolds)▫ stimulation of certain areas in the brain stem was known to

decrease the neuronal transmission along the spinothalamictract

• Discovery of morphine receptors▫ they were known to be present in the brain stem areas

• Discovery of endogenous opioid peptides▫ eg. Endorphines, enkephalins, dynorphin

• Descending tracts involving opioid peptides as neurotransmitter were discovered

• These were known to modify (inhibit) pain impulse transmission at the first synapse at the substantiagelatinosa

Presynaptic inhibitionsubstance P

enkephalin

pain impulse

blocking of pain impulse

C fibre

Final pain perception depends on activity of the

•Ascending pain impulse transmitting tracts

•Descending pain modulatory(inhibitory) tracts

Theories of pain

There is a single pathway for touch and pain

Less intensity produces touch

Increased intensity produces pain

There are two different pathways for touch and pain

Specificity theory

touch pain

Intensity theory

touch

pain

Gate control theory

• First described by P.D. Wall & Melzack (1965)

• “There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a gating mechanism

Gate control theory

When pain fibre is stimulated, gate will be opened & pain is felt

pain

pain is felt

+gate is opened

Gate control theory

When pain and touch fibres are stimulated together, gate will be closed & pain is not felt

pain is

not felt

touch

pain

+ -

gate is closed

• This theory provided basis for various methods of pain relief▫ Massaging a painful area

▫ Applying irritable substances to a painful area (counter-irritation)

▫ Transcutaneous Electrical Nerve Stimulation (TENS)

▫ Acupuncture ?

WDR (wide dynamic range cells)

• It is known that some of the second order neurons of the pain pathway behave as wide dynamic range neurons

• They are responsive to several somatosensory modalities (thermal, chemical and mechanical)

• They can be stimulated by pain but inhibited by touch stimuli

• WDR cells may represent neurons having pain as well as touch input

Referred pain

• sometimes pain arising from viscera are not felt at the site of origin but referred to a distant site.▫ eg.

cardiac pain referred to the left arm

diaphargmatic pain referred to the shoulder

▫ this paradoxical situation is due to an apparent error in localisation

PHYSIOLOGICAL EFFECTS OF PAIN

Pulmonary

(Dec lung

volume)

Atelectasis

Ventilation perfusion mismatch

Arterial hypoxemia

Hypercarbia

pneumonia

CVS(SNS Stim) HTN

Tachycardia

Myocardial Ischemia

Cardiac Dysrhythmia

Endocrine

system

Hyperglycemia

Sodium & water retention

Protein catabolism

Immune system Decreased immune function

Coagulation

system

Increased platelet adhesiveness

Decreased fibrinolysis

Hypercoagulation

DVT

GI system Ileus

Genitourinary

system

Urinary retention