This document provides an overview of the physiology of pain. It discusses the definition of pain, the dual nature of fast and slow pain, pain stimuli and receptors, nerve pathways carrying pain signals to the brain, brain areas involved in pain perception, descending pain modulatory pathways, and neurochemicals involved in pain pathways. It summarizes different types of pain such as neuropathic pain and nociceptive pain. The gate control theory of pain and modifications to this theory are also briefly described.
Knowledge of pain physiology is very important in understanding of electrotherapy prescription. So, this slide may be useful in understanding the background of the pain processes.
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Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.
Pain Physiology Presented At St Thomases Hospital 2.3.07London Pain Clinic
Pain Physiology.
Presented At St Thomases Hospital for trainee Anaesthetists as part of their FRCA (Fellow of the Royal College of Anaesthetists) examination preparations.
2nd March 2007
Gait control theory of pain given by Melzack & Wall in 1965. This is very much helpful for those medical/paramedical professionals who deal with subjects having pain.
Physiology of Pain (PPT) Nervous System PhysiologyShaista Jabeen
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
https://www.facebook.com/ShaistaJabeeen/
https://www.facebook.com/Human-Physiology-Lectures-100702741804409/
Physiology of Pain (PPT)
Nervous System Physiology
INTRODUCTION
BENEFITS OF PAIN SENSATION
COMPONENTS OF PAIN SENSATION
PATHWAYS OF PAIN SENSATION
FROM SKIN AND DEEPER STRUCTURES
FROM FACE
FROM VISCERA
FROM PELVIC REGION
VISCERAL PAIN
CAUSES OF VISCERAL PAIN
REFERRED PAIN
DEFINITION
EXAMPLES OF REFERRED PAIN
MECHANISM OF REFERRED PAIN
NEUROTRANSMITTERS INVOLVED IN PAIN SENSATION
ANALGESIA SYSTEM
ANALGESIC PATHWAY
GATE CONTROL THEORY
APPLIED PHYSIOLOGY
Short Notes
pdf ppt
https://userupload.net/s5uyonki1n7m
Pain is a somatic and emotional sensation which is unpleasant in nature and associated with actual or potential tissue damage. Physiologically, the function of pain is critical for survival and has a major evolutionary advantage. This is because behaviours which cause pain are often dangerous and harmful, therefore they are generally not reinforced and are unlikely to be repeated.
Knowledge of pain physiology is very important in understanding of electrotherapy prescription. So, this slide may be useful in understanding the background of the pain processes.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.
Pain Physiology Presented At St Thomases Hospital 2.3.07London Pain Clinic
Pain Physiology.
Presented At St Thomases Hospital for trainee Anaesthetists as part of their FRCA (Fellow of the Royal College of Anaesthetists) examination preparations.
2nd March 2007
Gait control theory of pain given by Melzack & Wall in 1965. This is very much helpful for those medical/paramedical professionals who deal with subjects having pain.
Physiology of Pain (PPT) Nervous System PhysiologyShaista Jabeen
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
https://www.facebook.com/ShaistaJabeeen/
https://www.facebook.com/Human-Physiology-Lectures-100702741804409/
Physiology of Pain (PPT)
Nervous System Physiology
INTRODUCTION
BENEFITS OF PAIN SENSATION
COMPONENTS OF PAIN SENSATION
PATHWAYS OF PAIN SENSATION
FROM SKIN AND DEEPER STRUCTURES
FROM FACE
FROM VISCERA
FROM PELVIC REGION
VISCERAL PAIN
CAUSES OF VISCERAL PAIN
REFERRED PAIN
DEFINITION
EXAMPLES OF REFERRED PAIN
MECHANISM OF REFERRED PAIN
NEUROTRANSMITTERS INVOLVED IN PAIN SENSATION
ANALGESIA SYSTEM
ANALGESIC PATHWAY
GATE CONTROL THEORY
APPLIED PHYSIOLOGY
Short Notes
pdf ppt
https://userupload.net/s5uyonki1n7m
Pain is a somatic and emotional sensation which is unpleasant in nature and associated with actual or potential tissue damage. Physiologically, the function of pain is critical for survival and has a major evolutionary advantage. This is because behaviours which cause pain are often dangerous and harmful, therefore they are generally not reinforced and are unlikely to be repeated.
1. Physiology of pain
Prof. Vajira Weerasinghe
Professor in Neurophysiology, Faculty of Medicine, University of Peradeniya &
Consultant Neurophysiologist, Teaching Hospital, Peradeniya
www.slideshare.net/vajira54
2. Topics covered in the lecture
1. What is pain? (International definition of pain)
2. Dual nature of pain: fast pain and slow pain
3. What causes pain : pain stimuli
4. Nerve pathways carrying pain signals to the brain
5. Brain areas involved in pain perception
6. Pain modulatory pathways
7. Neurochemicals involved in pain pathways
3. What is pain?
• Pain is a difficult word to define
• Patients use different words to
describe pain
• eg.
• Aching, Pins and needles, Annoying, Pricking, Biting, Hurting,
Radiating, Blunt, Intermittent, Burning, Sore, Miserable, Splitting,
Cutting, Nagging, Stabbing, Crawling, Stinging, Crushing, Tender,
Dragging, Numbness, Throbbing, Dull, Overwhelming, Tingling,
Electric-shock like, Penetrating, Tiring, Excruciating, Piercing,
Unbearable
• Different words in Sinhala or in Tamil
4. What is pain?
• 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
5. What is pain?
• Pain is
– subjective
– protective
– and it is modified by developmental, behavioural,
personality and cultural factors
• It is a symptom
• Associated signs are crying, sweating,
increased heart rate, blood pressure,
behavioural changes etc
6. Measurement of pain
• It is difficult to describe pain although we know
what it is
• It is difficult to measure pain
– visual analogue scale (VAS) is used
7. Dual nature of pain
• Fast pain
– acute
– pricking type
– well localised
– short duration
– Thin myelinated nerve
fibres are involved (A
delta)
• Slow pain
– chronic
– throbbing type
– poorly localised
– long duration
– Unmyelinated nerve fibres
are involved (c fibres)
8. 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
•Allodynia
•Pain caused by a lesion or disease of the
somatosensory nervous system
•Neuropathic pain
9. Pain terminology
International Association for the Study of Pain 2011
• 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
10. Pain terminology
International Association for the Study of Pain 2011
• 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.
11. Pain
• Pain as a sensation
– physiologically (nociception)
– Nociceptive pain
• Pain as an emotional experience
– Psychologically
– Psychogenic pain
• Pain caused by damage to nerve
– Neuropathic pain
12. Transduction and perception
• Transduction
– Process of converting noxious stimulus to action
potentials
• Perception
– Central processing of nociceptive impulses in order
to interpret pain
13. Stimuli
• Physical
– pressure etc
• Electrical
• Thermal
– cold, hot
• Chemical
– H+, lactic acid, K+, histamine, bradykinin, serotonin, leucotrines,
acetylcholine, proteolytic enzymes, capsaicin
– Prostaglandins (PGE2)
• Cannot directly stimulate nociceptors
• Increase the sensitivity of nociceptors for other stimuli (decrease the
threshold)
14. Receptors
There are no specialised receptors
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
15. Receptors
• Nociceptors are very slowly adapting type
• 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
16. Nerve pathways carrying pain signals to
the brain
• 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
18. central connections
• afferent fibre enters the spinal cord
• synapses in laminae ii,iii
– 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
21. Pain perception
• This occurs at different levels
– 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
22. Pathophysiology of pain
• Pain sensations could arise due to
– Inflammation of the nerves (neuritis)
– Injury to the nerves and nerve endings with scar
formation (disk prolapse)
– Injury to the structures in the spinal cord, thalamus
or cortical areas that process pain information
(spinal trauma)
– Abnormal activity in the nerve circuits that is
perceived as pain (phantom limb pain)
– Nerve invasion, for example by cancer (brachial
plexopathy)
23. Descending pain modulatory system
• several lines of experimental evidence
show the presence of 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 spinothalamic tract
– discovery of morphine receptors
– they were known to be present in the brain stem
areas
– discovery of endogenous opioid peptides
• eg. Endorphines, enkephalins, dynorphin
25. opioid peptides
• short peptides originally known to be secreted
in CNS and later found to be present in GIT etc
26. opioid peptides
∀ β endorphin
• Earliest to discover, present in pituitary
• Enkephalins or encephalins - met & leu
• widely distributed
• Dynorphin
• Endomorphine 1 & 2
• Pronociceptins
Receptors: mu, kappa, delta, recently discovered ORL1
receptor
27. • descending tracts involving opioid peptides as
neurotransmitter were discovered
• these were known to modify (inhibit) pain
impulse transmission at the first synapse at the
substantia gelatinosa
28. • first tract was discovered in 1981 by Fields and
Basbaum
– it involves enkephalin secreting neurons in the
reticular formation
– starting from the PAG (periaqueductal grey area) of
the midbrain
– ending in the NRM (nucleus raphe magnus) of the
medulla
– from their ending in the substantia gelatinosa of the
dorsal horn
29. • in the subtantia gelatinosa
– enkephalin secreting neuron is involved in
presynaptic inhibition of the pain impulse
transmission by blocking substance P release
33. • since then various other descending tracts
were discovered
• all of them share following common features
– involved in brain stem reticular areas
– enkephalins act as neurotransmitters at least in
some synapses
– most of these tracts are inhibitory
– midbrain nuclei are receiving inputs from various
areas in the cortex, subcortical areas, limbic
system, hypothalamus etc
– the ascending tract gives feedback input to the
descending tracts
– recently even nonopioid peptides are known to be
involved
34. sensorycortex
C fibre
Final pain perception
depends on activity
of the
Ascending
pain impulse
transmitting
tracts
Descending
pain modulatory
(inhibitory) tracts
35. 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
36. Gate control theory
• This explains how pain can be relieved very quickly by
a neural mechanism
• 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’
37. Gate control theory
When pain fibre is stimulated, gate will be opened & pain is felt
pain
pain is felt
+
gate is
opened
38. 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
39.
40. Gate control theory
• 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 ?
41. Gate control theory
• But the anatomcal basis for all the connections
of Wall’s original diagram is lacking
?
?
42. 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
43. WDR (wide dynamic range cells)
C fibre A fibre
pain &
mech mech
inhibitory
excitatory
WDR cell
44. WDR cells
• have been found in
– Spinal cord
– Trigeminal nucleus
– Brain stem
– Thalamus
– Cortex
45. Modifications to the gate control theory
• this could be modified in the
light of enkephalin activity
and WDR cells
• inhibitory interneuron may be
substantia gelatinosa cell
• descending control is more
important
• WDR cells may represent
neurons having pain as well
as touch input
46. 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
47. referred pain - theories
• convergence theory
– somatic & visceral structures
converge on the same
dermatome
– generally impulses through
visceral pathway is rare
– centrally brain is programmed
to receive impulses through
somatic tract only
– therefore even if the visceral
structure is stimulated brain
misinterpret as if impulses are
coming from the somatic
structure
visceral
somatic
second
order
neuron
++
++
+
+
+
48. referred pain - theories
• facilitatory theory
– somatic & visceral structures
converge on the same
dermatome
– stimulation of visceral
structure facilitates
transmission through somatic
tract
visceral
somatic
second
order
neuron
++
++
+
+
+
49. Pain memory
• Memory of pain often overshadows its primary experience in its
impact upon pathophysiology and human suffering
• The memory of pain can be more damaging than its initial
experience
• Central sensitization
– Increased responsiveness of nociceptive neurons in the central nervous
system to their normal or subthreshold afferent input
• Peripheral sensitization
– Increased responsiveness and reduced threshold of nociceptive neurons
in the periphery to the stimulation of their receptive fields
• Clinical interventions to blunt both the experience and
persistence of pain or to lessen its memory are now applied
50. • hypoxia / pressure / inflating a BP cuff
– first affect large A fibres (touch & pressure sense)
– then affect Aδ fibres (temperature sense & pricking
pain)
– lastly C fibres (burning pain)
local anaesthetics
– first relieve burning pain ( C fibres)
– then temperature sense & pricking pain (Aδ fibres)
– lastly touch& pressure sensation (large A fibres)
51. Pain arising from abdominal
viscera
• Mediated by C fibres
• Mainly due to the sensations of distention, muscular contraction, inflammation, hypoxia but not
to cutting, tearing, local irritation, burning
• Typically vague, dull, and nauseating
• These structures are innervated by autonomic nerve fibers
• It is poorly localized and tends to be referred to areas corresponding to the embryonic origin of
the affected structure
– stomach, duodenum, liver and pancreas referred to upper abdomen
– small intestines, proximal colon and appendix referred to periumbilical pain
– distal colon and GU tract referred to lower abdominal pain
• Peritonitis causes somatic pain
• Diffuse localization of true visceral pain is probably due to the low density of visceral sensory
innervation and extensive divergence of the visceral input within the central nervous system
52. Capsaicin and vanniloid receptors
• Active compound in chilies is capsaicin
• Capsaicin chemically is one of the vanilloids
• Capsaicin receptor is called TRPV1
– (Transient receptor potential vanilloid type 1)
• This receptor is also stimulated by
– heat greater than 43°C
– low pH
• This receptor is sensitised by prostaglandins and bradykinins
• Upon prolonged exposure to capsaicin TRPV1 activity decreases
– this phenomenon is called desensitization
– Extracellular calcium ions are required for this phenomenon
– This causes the paradoxical analgesic effect of capsaicin
53. Cannabinoid receptor
• Cannabis (marijuvana or ganja) causes pain relief
• Cannabis act on cannabinoid receptors found in pain
pathway
• There are endocannabinoids as well
• Cannabinoid receptor-related processes are involved
in cognition, memory, anxiety, control of appetite,
emesis, motor behavior, sensory, autonomic and
neuroendocrine responses, immune responses and
inflammatory effects
54. Summary
• Pain is not just a sensation but is a more complex
phenomenon
• Pain can be blocked at many places
• Chemicals play an important role in causing pain as
well as in reducing pain
• Neural mechanisms also play a role in pain interaction
• This complex nature of pain perception makes it a
very difficult entity to control
55. “Pain is a more terrible lord
of mankind than even death
itself”
Dr. Albert Schweitzer (1875-1965)