Pain Physiology Pathology

Pain physiology & pathologyPain physiology & pathology

Dr . Keerthi

Dept. of Anaesthesiology

•• PainPain is a complex unpleasant phenomenon is a complex unpleasant phenomenon composed of composed of sensorysensory experiences that include experiences that include time, space, time, space, intensity, intensity, emotion, cognition, and motivationemotion, cognition, and motivation

•• PainPain is an unpleasant or emotional experience is an unpleasant or emotional experience originating in real or potential damaged tissueoriginating in real or potential damaged tissue The International Association for the Study of PainThe International Association for the Study of Pain

•• PainPain is an unpleasant phenomenon that is an unpleasant phenomenon that is is

uniquely uniquely experiencedexperienced by each individualby each individual; it cannot be ; it cannot be adequately adequately defined, defined, identified, or measured by an observeridentified, or measured by an observer

Definitions of pain

The experience of painThe experience of pain

Three systems interact usually to produce pain:Three systems interact usually to produce pain: 1.1. sensory -sensory - discriminativediscriminative

2. motivational - affective2. motivational - affective

3. cognitive - evaluative3. cognitive - evaluative

1. 1. Sensory - discriminative systemSensory - discriminative system processes information about processes information about tthehe strength, intensity, strength, intensity, quality quality and temporal and spatial and temporal and spatial aspects of painaspects of pain

2. 2. Motivational - affective systemMotivational - affective system determines the individual´s determines the individual´s approach-avoidance behavioursapproach-avoidance behaviours

3. 3. Cognitive - evaluative systemCognitive - evaluative system overlies the individuals learnedoverlies the individuals learned

behaviour concerning the experience of pain. behaviour concerning the experience of pain. It It may block, may block,

modulate, or enhance the perception of painmodulate, or enhance the perception of pain

Pain Pain cclassification;lassification;

1.1. Somatogenic painSomatogenic pain is pain with cause (usually known)is pain with cause (usually known) localised in the body tissuelocalised in the body tissue a/ nociceptive paina/ nociceptive pain b/ neuropatb/ neuropathhic painic pain

22. . Psychogenic painPsychogenic pain is pain for which there is no known is pain for which there is no known physical causephysical cause but processing of sensitive information but processing of sensitive information in CNS is dysturbedin CNS is dysturbed

Clinically Acute and Clinically Acute and cchronic hronic ppainain

Acute painAcute pain is a protective mechanism that alerts the is a protective mechanism that alerts the

individual to a condition or experience that is immediately individual to a condition or experience that is immediately

harmful to the bodyharmful to the body

OnsetOnset - - usually suddenusually sudden

Relief Relief -- after the chemical mediators that stimulate the after the chemical mediators that stimulate the nociceptorsnociceptors,, are removed are removed

•• This type of pain mobilises the individual to prompt action This type of pain mobilises the individual to prompt action to relief itto relief it

•• Stimulation of autonomicStimulation of autonomic nervous system can be observed nervous system can be observed during this type of painduring this type of pain ((mydriasis, tachycardia, tachypnoe, mydriasis, tachycardia, tachypnoe,

sweating, vasoconstriction)sweating, vasoconstriction)

Responses to acute painResponses to acute pain

- increased heart rate - - increased heart rate - diaphoresisdiaphoresis

- increased respiratory rate - - increased respiratory rate - blood sugar blood sugar

- elevated blood pressure - - elevated blood pressure - gastric acid gastric acid

secretionsecretion

- pallor or flushing- pallor or flushing,, - - gastric motility gastric motility dilated pupilsdilated pupils -- blood flow to the blood flow to the visceraviscera, ,

kidney kidney and skinand skin - - nausea occasionallynausea occasionally occursoccurs

Psychological and behavioural response to acute Psychological and behavioural response to acute painpain

- fear fear - general sense of unpleasantness o- general sense of unpleasantness orr unease unease

- anxiety- anxiety

Chronic painChronic pain is persistentis persistent or intermittent or intermittent usually usually

defined as lasting at least defined as lasting at least 6 months6 months

The cause is often unknownThe cause is often unknown, , often develops insidiously, often develops insidiously,

vvery ery often is associated with a sense of hopelessness often is associated with a sense of hopelessness

and and

helplessness.helplessness. Depression often resultsDepression often results

Psychological response to chronic painPsychological response to chronic pain

Intermittent painIntermittent pain produces a physiologic response produces a physiologic response similar to acute pain.similar to acute pain.

Persistent painPersistent pain allows for allows for adaptation adaptation (functions of the (functions of the body are normal but the pain is not reliefed)body are normal but the pain is not reliefed)

Chronic pain producesChronic pain produces significant behavioural and significant behavioural and

psychological changespsychological changes

The main changes are:The main changes are:

- - depression depression

- an attempt to keep pain - related behaviour- an attempt to keep pain - related behaviour to a to a

minimumminimum

- sleeping disorders- sleeping disorders

- - preoccupation with the pain preoccupation with the pain

- tendency to deny pain- tendency to deny pain

Pain Pain tthreshold and hreshold and ppain ain ttoleranceolerance

The pain threshold The pain threshold is the point at which a stimulus is perceivedis the point at which a stimulus is perceivedas painas painIt does not vary significantly among It does not vary significantly among healthy healthy people or in the same people or in the same person over time person over time

PPerceptual dominanceerceptual dominance-- iintense pain at one location may cause ntense pain at one location may cause

an increase in the pain threshold in another locationan increase in the pain threshold in another location

• The pain tolerance is expressed as duration of time or the

intensity of pain that an individual will endure before

initiation

overt pain responses.

It is influenced by - persons cultural prescriptions - expectations - role behaviours - physical and mental health

•• Pain tolerancePain tolerance is generally is generally decreaseddecreased::

-- with repeated exposure to pain, with repeated exposure to pain,

- - by fatigue, anger, boredom, apprehension, by fatigue, anger, boredom, apprehension,

- - sleep deprivationsleep deprivation

•• Tolerance to painTolerance to pain may be may be increasedincreased::

-- by alcohol consumption, by alcohol consumption,

- - medication, hypnosis, medication, hypnosis,

- - warmth, distracting activities, warmth, distracting activities,

- - strong beliefs or faith strong beliefs or faith

Pain tolerance Pain tolerance varies greatlyvaries greatly among people and in among people and in the samethe same person over timeperson over time

A decrease in pain tolerance is also evident in the A decrease in pain tolerance is also evident in the

elderly, elderly,

and women appear to be more and women appear to be more tolerant tolerant to pain than to pain than

menmen

Age anAge andd pperception of erception of ppainain

Children and the elderlyChildren and the elderly may experience or express pain may experience or express pain

differently than adults differently than adults

InfantsInfants in the first 1 to 2 days of life are in the first 1 to 2 days of life are less sensitiveless sensitive to to

pain pain

(or they simply lack the ability to verbalise the pain (or they simply lack the ability to verbalise the pain

experience).experience).

A full behavioural response to pain is apparent at 3 to 12 A full behavioural response to pain is apparent at 3 to 12

month of life month of life

Older childrenOlder children,, between the ages of 15 and 18 years, between the ages of 15 and 18 years, tend to have a lower pain threshold than do adultstend to have a lower pain threshold than do adults

Pain threshold tends to increase with ageingPain threshold tends to increase with ageing

This change is probably caused by peripheral neuropathies This change is probably caused by peripheral neuropathies

and changes in the thickness of the skinand changes in the thickness of the skin

Neuroanatomy of Neuroanatomy of ppainain

The portions of the nervous system responsible for the The portions of the nervous system responsible for the

sensation and perception of pain may be divided into three sensation and perception of pain may be divided into three

areas:areas:

1.1. afferent pathwaysafferent pathways

2.2. CNSCNS

3.3. efferent pathwaysefferent pathways

The afferent portionThe afferent portion is composed of:is composed of:

a) nociceptors (pain receptors)a) nociceptors (pain receptors)

b) afferent nervb) afferent nerv fibres fibres

c) spinal cord networkc) spinal cord network

NOCICEPTORS

• Cutaneous mechanoreceptors– Respond to nondiscriminative tactile stimuli– Pinch, rub, stretch, squeeze– A-delta and C fiber, high-threshold

• Cutaneous thermoreceptors– Respond to transient change in temperature– Innocuous warm and cool stimuli

Deep Nociceptors

• Muscle nociceptors – GIII, GIV afferents– Bradykinin

– 5-HT (Inflammation releases 5-HT in TMJD)

– K+

– GLUT

• Joint nociceptors – GIII, GIV afferents– Inflammation (K+, Bradykinin, 5-HT, GLUT)

– Kaolin (experimental models)

– Carregeenan (experimental models)

Visceral Nociceptors

• Heart – A-delta and C afferents– H+– K+– Ischemia– Bradykinin– PGE-2

Lung Nociceptors

• Lung Irritant Receptors – A-delta afferents– Irritant aerosols and gases– Mechanical stimuli

• Lung “J” Receptors – C-fibers– Capsaicin– Pulmonary congestion, edema– Inhaled irritants

G.I. Tract Nociceptors

• Rapidly-adapting mechanoreceptors, slowly adapting mechanoreceptors, chemoreceptors (A-delta and C-fibers)– Irritation of the mucosa– Distension– Powerful contraction– Torsion– Traction– Bloating– Cramping– Appendicitis– Impaction

Distribution of Nociceptors

• UG Tract - C-polymodal (e.g., testis)– Intense mechanical stimuli– Noxious heat– Algesic chemicals

• Bone - periosteum• Blood Vessels - walls• Brain – none

– C-fibers in dura mater

CNS Neurotransmittersof A-delta and C-fibers

• Substance P (Neuropeptide)

• Calcitonin Gene Realted Peptide (CGRP)

• Excitatory amino acids – e.g., glutamate– Release in ischemia/hypoxia - neurotoxicity

Membrane Receptors ofA-delta and C-fibers in CNS

• Purinergic (ATP)

• GABA-ergic

• Mu opioid receptor (MOR)

Types of Nerves

• Afferent (Ascending) – transmit impulses from the periphery to the brain– First Order neuron– Second Order neuron– Third Order neuron

Peripheral and Central Pathways for PainAscending TractsAscending Tracts Descending TractsDescending Tracts

Cortex

Midbrain

Medulla

Spinal Cord

Thalamus

Pons

First Order Neurons• Stimulated by sensory receptors• End in the dorsal horn of the spinal cord• Types

– A-alpha – non-pain impulses– A-beta – non-pain impulses

• Large, myelinated• Low threshold mechanoreceptor; respond to light touch &

low-intensity mechanical info– A-delta – pain impulses due to mechanical pressure

• Large diameter, thinly myelinated• Short duration, sharp, fast, bright, localized sensation

(prickling, stinging, burning)– C – pain impulses due to chemicals or mechanical

• Small diameter, unmyelinated• Delayed onset, diffuse nagging sensation (aching,

throbbing)• a

Second Order Neurons• Receive impulses from the FON in the dorsal horn

– Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve

• T Cells (transmission cells): transmission cell that connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain

– Travel along the spinothalmic tract – Pass through Reticular Formation

• Types– Wide range specific

• Receive impulses from A-beta, A-delta, & C

– Nociceptive specific• Receive impulses from A-delta & C

• Ends in thalamus

Third Order Neurons

• Begins in thalamus

• Ends in specific brain centers (cerebral cortex)– Perceive location, quality, intensity– Allows to feel pain, integrate past experiences

& emotions and determine reaction to stimulus

The portion of CNSThe portion of CNS involved in the involved in the interpretation ofinterpretation of

thethe pain signals are thepain signals are the limbic system, limbic system,

reticular reticular

formation,formation, thalamus, hypothalamus and cortexthalamus, hypothalamus and cortex

●● The efferentThe efferent pathwayspathways, , composed of the fiberscomposed of the fibers connectingconnecting thethe reticular formation, midbrain,reticular formation, midbrain, andand substantia gelatinosasubstantia gelatinosa,, areare responsible forresponsible for modulatingmodulating pain sensationpain sensation

The brain first perceives the sensation of painThe brain first perceives the sensation of pain

•• The thalamus, The thalamus, sensitive sensitive cortex :cortex :

perceivingperceiving

describing describing of painof pain

localisinglocalising

•• Parts of thalamus, brainstem and reticular formation:Parts of thalamus, brainstem and reticular formation: - - identify dull longer-lasting, and diffuse painidentify dull longer-lasting, and diffuse pain

•• The reticular formation and limbic system:The reticular formation and limbic system:

- - control the emotional and affective response to control the emotional and affective response to

painpain

Because the cortex, thalamus and brainstem arBecause the cortex, thalamus and brainstem aree

interconnected with the hypothalamus and autonomic interconnected with the hypothalamus and autonomic

nervous system, thenervous system, the perception ofperception of pain is associated pain is associated

with anwith an

autonomic response autonomic response

Descending Neurons• Descending Pain Modulation (Descending Pain Control

Mechanism)• Transmit impulses from the brain (corticospinal tract in the

cortex) to the spinal cord (lamina)– Periaquaductal Gray Area (PGA) – release enkephalins– Nucleus Raphe Magnus (NRM) – release serotonin

– The release of these neurotransmitters inhibit ascending neurons

• Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes analgesia.

• Endogenous opioid peptides - endorphins & enkephalins

The The rrole of the ole of the aafferent and fferent and eefferent fferent ppathwaysathways in in

processing of pain informationprocessing of pain information

Nociceptive painNociceptive pain

Nociceptors:Nociceptors: EndEndingings of small unmyelinated and lightly s of small unmyelinated and lightly myelinated afferent neuronsmyelinated afferent neurons

Stimulators:Stimulators: CChemical, mechanical and thermal hemical, mechanical and thermal noxaenoxaeMild stimulationMild stimulation positive, pleasurable positive, pleasurable

sensationsensation (e.g. tickling)(e.g. tickling)

Strong stimulationStrong stimulation pain pain

ThTheseese differences are a result of the differences are a result of the frequency frequency and amplitudeand amplitude of the afferent signal of the afferent signal transmittedtransmitted from the nerve endingsfrom the nerve endings to the CNS to the CNS

LocationLocation: : IIn muscles, tendons, epidermisn muscles, tendons, epidermis,, subcutanous subcutanous

tissue,tissue, visceral organsvisceral organs

- - they are not evenly distributed in the bodythey are not evenly distributed in the body (in skin more than in internal structures(in skin more than in internal structures))

Injury response

Nociceptive pain:

Afferent pathwaysAfferent pathways::

•• From From nociceptorsnociceptors transmitted transmitted by by small A-delta fibers and small A-delta fibers and

CC-- fibers fibers to the spinal cordto the spinal cord form synapses with neurons form synapses with neurons

in the dorsal hornin the dorsal horn(DH)(DH)

•• From From DH DH transmitted to higher parts of the spinal cordtransmitted to higher parts of the spinal cord

and to the rest of the and to the rest of the CNS CNS by spinothalamic tractsby spinothalamic tracts

**TheThe small unmyelinated Csmall unmyelinated C-- neurons neurons are responsible for the are responsible for the

transmission oftransmission of diffuse burning or aching sensationsdiffuse burning or aching sensations

**Transmission through the Transmission through the larger, myelinated Alarger, myelinated A- delta- delta fibers fibers

occurs much more quickly. Aoccurs much more quickly. A - - fibers carry fibers carry well-localized, well-localized,

sharp pain sensationssharp pain sensations

Figure 13-8 - Overview

EEfferent analgesic systemfferent analgesic system

Its role: - Its role: - inhibition of afferent pain signalsinhibition of afferent pain signals

Mechanisms:Mechanisms:

- pain a- pain afferentfferentss stimula stimulatestes the neuronsthe neurons in in

periaqueductal periaqueductal

graygray ((PAGPAG) -) - gray matter surroundinggray matter surrounding the cerebral the cerebral

aqueductaqueduct in the midbrain results inin the midbrain results in activation activation of of

efferentefferent

(descendent) anti-nociceptive(descendent) anti-nociceptive pathways pathways

- - ffrom there the impulserom there the impulsess areare transmitted through transmitted through thethe spinalspinal cord tocord to the dorsal hornthe dorsal horn

- - there thaythere thay inhibit or block transmission of inhibit or block transmission of

nociceptive nociceptive signals at the level of dorsal hornsignals at the level of dorsal horn

Descendent antinociceptive systémDescendent antinociceptive systém

Enk – enkefalinergicPAG – paraaqueductal grayEAA – excitatory amino acidsRVM – rostral ventro-medial medulla

Control of Nociceptive Inputs and Modulation of Pain

• The brain is able to modulate all the varieties of sensation via efferent connections to receptors or neurons in sensory pathways. This is also true for nociception and there are three (non-mutually exclusive) mechanisms by which nociceptive inputs are modulated.

Gate Control Theory of Pain• Large-diameter primary afferent fibers (Aα and Aβ fibers)

can inhibit, via inhibitory interneurons, dorsal horn neurons (projection neurons) that give rise to spinothalamic tract fibers.

• This form of control of nociceptive input is known as the gate control theory of Melzack and Wall, after the scientists who proposed it. Electrical stimulation of the dorsal columns or of large, myelinated peripheral nerve fibers by transcutaneous electrical nerve stimulation (TENS) may relieve pain by this mechanism. Acupuncture anesthesia may also be an example of dorsal column-anterolateral system interaction since it is reported to be effective only when needles are inserted near bundles of Group II fibers. Dorsal column-anterolateral system interactions may occur at several levels, including spinal cord dorsal horn, spinal V nucleus, and thalamus.

Gate Control Theory of Pain

• Pain and temperature signals cause C and A-delta fibers to release an excitatory neurotransmitter (e.g., glutamate, SP) and stimulate second order neurons directly

• Pain and temperature signals also cause C and A-delta fibers to release an inhibitory neurotransmitter (e.g., GABA, enkephalin) and inhibit an inhibitory interneuron, thereby, opening the gate for transmitting pain and temperature signals to second order neurons

• Tactile signals cause A-fibers to release an excitatory neurotransmitter and stimulate the inhibitory interneuron which closes the gate for transmitting pain and temperature signals to second order neurons

• Tactile stimulation such as stroking, massaging or kissing an affected area closes the gate and raises the pain threshold

Role of Enkephalins and Endorphins in Modulating Pain

• Enkephalins and endorphins are naturally occurring brain peptides with an opiate-like effect on pain transmission. Certain inhibitory interneurons in the dorsal horn use enkephalin as a neurotransmitter.

• The interneurons are activated by serotonergic fibers that descend from the reticular formation. Enkephalin causes a decrease in the EPSP produced by the nociceptor via a presynaptic inhibitory action. In part, the effect is due to a decrease in the duration of the action potential in the C fiber terminal. When that occurs, less glutamate (GLU) and substance P are released from the terminal.

Role of Serotonin and Norepinephrine

• Reticulospinal fibers from raphe nuclei project to dorsal horn of spinal cord and release serotonin which stimulates interneurons to release enkephalin

• Enkephalin inhibits transmission of pain and temperature signals in second order neurons

• Reticulospinal fibers from locus ceruleus also project to dorsal horn of spinal cord and release norepinephrine which inhbits pain and temperature signals by an unknown mechanism

• Mental illnesses such as depression decrease serotonin and norepinephrine and lower pain thresholds while antidepressant drugs and therapies (e.g., exercise) which increase serotonin and norepinephrine levels raise pain thresholds

Neuropathic PainNeuropathic pain is pain transmitted over damaged nerves. Patient Description of Neuropathic Pain:

•Burning, electric, searing, tingling, and migrating or traveling.

Causes of Neuropathic Pain: •Amputation, shingles (herpes zoster), AIDS (peripheral neuropathy), diabetic neuropathy, fibromyalgia, and cancers that affect the spinal cord, among others.

How Neuropathic Pain Happens

• When nerves become damaged or injured, they stop working properly– May send the wrong signal to the brain

– Injured nerves might tell the brain that your foot is experiencing burning pain even when you aren’t stepping on something hot

• Nerves can be injured or damaged in a number of ways, including a spinal cord injury or a medical condition such as diabetes, shingles or a stroke

Price SA. Pathophysiology: Clinical Concepts of Disease Processes. 5th ed; 1997

symptoms• Frequently results in a burning, tingling and

shock-like sensation

• Experience of pain to things that are often non-painful, such as to bed sheets or socks

• Pain can persist even after the cause has been removed

• Abnormal sensations that are described as “pins and needles”

• The symptoms can be mild to incapacitating and are often progressive

• Symptoms often worse at night

Wall PD. Textbook of Pain. 4th ed. 1999.; Dworkin RH, et al. Arch of Neuro. 2003;60:1524-1534; Jude EB. Clinics in Pod Med and Surg. 1999;16:81-97; Weiner RS. Pain Management: A Practical Guide for Clinicians. 6th ed. 2002; Galer BS. Neurol. 1995;45(Suppl 9):S17-S25.

Neuropathic Pain is Different from Muscle/skeletal Pain

Neuropathic Pain Muscle/skeletal Pain

Chronic pain (months/years) Acute pain (hours or days)

Caused by injury or disease to nerves Caused by injury or inflammation that affects both the muscles and joints

Mild to excruciating pain that can last indefinitely

Moderate to severe pain that disappears when the injury heals

Causes extreme sensitivity to touch –simply wearing light clothing is painful

Causes sore, achy muscles

Sufferers can become depressed or socially withdrawn because they see no relief in sight and may experience sleep

problems

Sufferers can become anxious and distressed but optimistic about relief

from pain

Wall PD. Textbook of Pain. 4th ed; 1999; Jude EB. Clin in Pod Med and Surg.1999;16:81-97; Price SA. Pathophysiology: Clinical Concepts of Disease Processes. 5th ed; 1997: Goldman L. Cecil Textbook of Medicine. 21st ed; 2000

Symptoms of Neuropathic Pain Characterized Differently

Neuropathic Pain Muscle/Skeletal Pain

Price SA. Pathophysiology: Clinical Concepts of Disease Processes. 5th ed; 1997; Galer BS et al. Diabetes Res Clin Pract. 2000;47:123-128

AllodyniaAllodynia - - phenomenon characterised by painful phenomenon characterised by painful

sensations provoked by nonsensations provoked by non--noxious stimuli, noxious stimuli,

((e.g. touche.g. touch)), transmitted by fast- conducting , transmitted by fast- conducting

nerve fibresnerve fibres

Mechanism:Mechanism: changes of the response characteristics of changes of the response characteristics of secosecond nd - order- order spinal neuronsspinal neurons so that normally so that normally

inactive orinactive or weak synaptic contact mediating weak synaptic contact mediating

nonnon--noxius stimulinoxius stimuli acquire the capability to acquire the capability to

activateactivate a neuron that normally responds onlya neuron that normally responds only

to impulses signaling painto impulses signaling pain

• Hypersensitivity – increased sensitivity of the system involved in the pain processing

• Hyperalgesia – increased the pain sensitivity to noxious stimuli

Hyperalgesia vs Allodynia

• Allodynia• Pain to stroking stimuli• A-beta fiber

mediated• Decreases with

ischemic block

• Hyperalgesia• Pain to punctate

stimuli (von Frey)• A-delta and C-fiber

mediated• Persists with

ischemic block

Most Most peripheral neuralgias are the result of trauma or peripheral neuralgias are the result of trauma or

surgerysurgery.. Such a conditions does not necessary occur as Such a conditions does not necessary occur as

a result of damageing a result of damageing aa major nerve trunkmajor nerve trunk but may be but may be

causedcaused by an by an incision involving only small nerve branchesincision involving only small nerve branches

(incisional pain)(incisional pain) MechanismMechanism: : the pain is due to the pain is due to neuroma formationneuroma formation in the in the

scar tissue (?)scar tissue (?)

Peripheral neuralgias after trauma or surgeryPeripheral neuralgias after trauma or surgery

Common forms of neuropathic painCommon forms of neuropathic pain

lumbosacral and cervical rhizotomy, lumbosacral and cervical rhizotomy,

● ● peripheralperipheral neuralgianeuralgia

pain following spinal cord injurypain following spinal cord injury

Incidence of severe pain due to spinal cord and cauda equina Incidence of severe pain due to spinal cord and cauda equina lesionslesions rangesranges from 35 to 92 % of patientsfrom 35 to 92 % of patients

This pain is ascribed to This pain is ascribed to 3 3 causescauses::

1. mechanically induced pain (fractur1. mechanically induced pain (fracturee bones, bones,

myofascial pain)myofascial pain)

2. radicular pain (compression of nerve root)2. radicular pain (compression of nerve root)

3. central pain (deaferentation mechanism)3. central pain (deaferentation mechanism)

Acute PainAcute PainWe can distinguish We can distinguish two two types of acute paintypes of acute pain::

1. Somatic1. Somatic

2. Visceral2. Visceral

– – rreferredeferred

Somatic pain is superficialSomatic pain is superficial coming from the skin or close to coming from the skin or close to the surface of the body.the surface of the body.

Visceral painVisceral pain refers to pain inrefers to pain in internal organs, the abdomen, internal organs, the abdomen, oorr chest chest..

Clinical Manifestation of PainClinical Manifestation of Pain

Different types of chronic somatic painDifferent types of chronic somatic pain

I. Nervous system intactI. Nervous system intact

1. nociceptive pain1. nociceptive pain

2. nociceptive - neurogenic pain2. nociceptive - neurogenic pain (nerve trunk pain(nerve trunk pain))

II. Permanent functional and/or morphological II. Permanent functional and/or morphological abnormalitiesabnormalities of the nervous systemof the nervous system (preganglionic, spinal - supraspinal)(preganglionic, spinal - supraspinal)

1. neurogenic pain1. neurogenic pain

2. neuropathic pain2. neuropathic pain

3. deafferentation pain3. deafferentation pain

The most commonThe most common chronic pain chronic pain

1.1. Persistent low back pain Persistent low back pain

– – result of poor muscle tone,inactivity, result of poor muscle tone,inactivity,

muscle strainmuscle strain, , sudden vigorous exercisesudden vigorous exercise

2. Chronic pain associated with cancer2. Chronic pain associated with cancer

3. Neuralgias3. Neuralgias - - results from damages of peripheral nervesresults from damages of peripheral nerves

a)a) CausalgiaCausalgia - - severe burning pain appearingsevere burning pain appearing 1 to 2 weeks after 1 to 2 weeks after

the nerve injury associated with discoloration and the nerve injury associated with discoloration and

changes in the texture of the skin in the affected changes in the texture of the skin in the affected

area.area.

b)b) Reflex sympathetic dystrophiesReflex sympathetic dystrophies - - occur after peripheral occur after peripheral

nerve injury and is characterised by nerve injury and is characterised by continuous continuous

seversevere e burning painburning pain.. Vasomotor changes are Vasomotor changes are

present (vasodilatationpresent (vasodilatation vasoconstriction vasoconstriction cool cool

cyanotic andcyanotic and edematous extremities).edematous extremities).

4. Myofascial pain syndromes4. Myofascial pain syndromes - - second most common cause second most common cause

of chronic pain.of chronic pain.

These conditions include: These conditions include: myositis, fibrositis, myalgia,myositis, fibrositis, myalgia,

musclemuscle strain, injury to the muscle and fasciastrain, injury to the muscle and fascia

The pain is a result ofThe pain is a result of muscle spasm, tenderness muscle spasm, tenderness and stiffnessand stiffness

5. Hemiagnosia5. Hemiagnosia

– – is a loss of ability to identify the source of pain onis a loss of ability to identify the source of pain on one one

side side

(the affected side) of the body(the affected side) of the body.. Application of painful Application of painful

stimulistimuli

to the affected side thus produces to the affected side thus produces anxiety, moaning, anxiety, moaning,

agitation agitation

and distressand distress but no attem but no attemppt to withdrawal fromt to withdrawal from or or

push asidepush aside

the offending stimulus. Emotional and autonomic the offending stimulus. Emotional and autonomic

responses responses

to the painto the pain my be intensified.my be intensified.

● ● Hemiagnosia is associated with stroke that produces Hemiagnosia is associated with stroke that produces

paralysis and hypersensitivity to painparalysis and hypersensitivity to painful stimuli ful stimuli in thein the

affected sideaffected side

6. Phantom limb pain6. Phantom limb pain - is pain that an individual feels in is pain that an individual feels in amputated limbamputated limb

Phantom Limb Pain

• Burning, shooting, or crushing pains may be experienced in the missing part following amputation. When triggered from the stump, they may be a type of neuroma pain. In other cases, a disorder of central processing is implicated.

Pathophysiology of muscle painPathophysiology of muscle pain

Muscle painMuscle pain -- a part ofa part of somatic deep painsomatic deep pain,,

(MP)(MP) - - it is commonit is common inin rheumatology and sports rheumatology and sports medicinemedicine

- - is rather diffuse and difficult to locateis rather diffuse and difficult to locate MPMP is not a prominent feature of the serious progressive diseases is not a prominent feature of the serious progressive diseases

affecting muscle, e.g. the muscular dystrophies, denervationaffecting muscle, e.g. the muscular dystrophies, denervation, ,

or metabolic myopathies,or metabolic myopathies, but it is a feature of rhabdomyolysisbut it is a feature of rhabdomyolysis Muscles are relatively insensitive to pain when elicited by needle Muscles are relatively insensitive to pain when elicited by needle prickprick or knife cutor knife cut, , but overlying fascia is but overlying fascia is very very sensitive to painsensitive to pain..

Events, processes which may lead to muscular pain are:Events, processes which may lead to muscular pain are: ● ● metabolic events:metabolic events: •• metabolic depletionmetabolic depletion (( ATP ATP muscular muscular contractcontracture)ure) •• accumulation of unwanted metabolitiesaccumulation of unwanted metabolities (K(K++, , bradykinin)bradykinin)

Pathophysiology of visceral painPathophysiology of visceral pain

Visceral pain:Visceral pain: TTypesypes - angina pectoris, myocardial infarction, acute - angina pectoris, myocardial infarction, acute

pancreatitis, cephalic pain, prostatic pain.pancreatitis, cephalic pain, prostatic pain.

Receptors:Receptors: unmyelinated C - fibresunmyelinated C - fibres

For human pathophysiology theFor human pathophysiology the kinds of stimuli apt to kinds of stimuli apt to induceinduce pain in the viscera are importantpain in the viscera are important. .

It is well-known that the stimuli likely to induce cutaneous It is well-known that the stimuli likely to induce cutaneous

pain are not algogenicpain are not algogenic inin the viscera. This explains why in the viscera. This explains why in

the past the viscera werethe past the viscera were considered to be insensitive considered to be insensitive

to painto pain

Adequate stimuliAdequate stimuli of inducing visceral pain:of inducing visceral pain:

1. abnormal distention and contraction of the hollow 1. abnormal distention and contraction of the hollow viscera muscle wallsviscera muscle walls 2. rapid stretching of the capsule of such solid visceral 2. rapid stretching of the capsule of such solid visceral

organs asorgans as liver, spleen, pancreas... liver, spleen, pancreas... 3. abrupt anoxemia of visceral muscles3. abrupt anoxemia of visceral muscles 4. formation and accumulation of pain - producing 4. formation and accumulation of pain - producing

substancessubstances 5. direct action of chemical stimuli (oesophagus, stomach5. direct action of chemical stimuli (oesophagus, stomach)) 6. traction or compression of ligaments and vessels6. traction or compression of ligaments and vessels

7. inflammatory processes7. inflammatory processes 8. necrosis of some structures (myocardium, pancreas)8. necrosis of some structures (myocardium, pancreas)

Characteristic feature of true visceral Characteristic feature of true visceral painpain

a) it is dull, deep, not well defined, and differently a) it is dull, deep, not well defined, and differently described by the patientsdescribed by the patients

b) b) sometimes sometimes it is difficult to locate this type of pain it is difficult to locate this type of pain because it because it tends to tends to iirrrradiateadiate

c) it is often accompanied by a sense of malaisec) it is often accompanied by a sense of malaise

d) it induces strong autonomic reflex phenomena d) it induces strong autonomic reflex phenomena (much more pronounced than in pain of somatic (much more pronounced than in pain of somatic origin) origin) -- diffuse sweating, vasomotor responses, changes diffuse sweating, vasomotor responses, changes of of

arterial pressure and heart rate, and an intense arterial pressure and heart rate, and an intense

psychic psychic

alarm reaction alarm reaction --"angor animi" - in angina "angor animi" - in angina

pectoris)pectoris)

•• There are There are many visceral sensation that are unpleasant but below many visceral sensation that are unpleasant but below the level of painthe level of pain, e.g. feeling of disagreeable fullness or acidity of the , e.g. feeling of disagreeable fullness or acidity of the stomach or undefined and unpleasant thoracic or abdominal stomach or undefined and unpleasant thoracic or abdominal sensation. sensation. These visceral sensation may precedeThese visceral sensation may precede the onset of visceral the onset of visceral painpain

Refered visceral pain (transferred pain)Refered visceral pain (transferred pain)

Refered painRefered pain = when an algogenic process affecting a = when an algogenic process affecting a

viscusviscus recursrecurs

frequently or becomes more intense and prolonged, the frequently or becomes more intense and prolonged, the

locationlocation

becomes more exact and the painfull sensation isbecomes more exact and the painfull sensation is progressively progressively

felt infelt in

more superficial strufturesmore superficial struftures

●● Refered pain may be accompanied by allodynia and Refered pain may be accompanied by allodynia and

cutaneouscutaneous and muscular hyperalgesiaand muscular hyperalgesia

Mechanisms involved in refered pain creation:Mechanisms involved in refered pain creation: a) a) convergence of impulses from viscera and from the skinconvergence of impulses from viscera and from the skin in the CNS:in the CNS:

Sensory impulses from the viscera create an irritable focusSensory impulses from the viscera create an irritable focus in the in the segment at which they enter the spinal cord.segment at which they enter the spinal cord. Afferent impulses from the Afferent impulses from the

skin entering the same segment are therebyskin entering the same segment are thereby facilitated, giving rise to true facilitated, giving rise to true cutaneous pain.cutaneous pain.

b) senzitization of neurons in dorsal hornb) senzitization of neurons in dorsal horn

Referred PainPains is perceived at a site distant from the source.Visceral damage

Painful vPainful visceral afferent impulses isceral afferent impulses activate anterior activate anterior horn horn

motor cells to produce rigidity of the muscle motor cells to produce rigidity of the muscle

(visceromotor (visceromotor

reflexes)reflexes)

A similar activation of A similar activation of anterolateral autonomic cells anterolateral autonomic cells

induces induces pyloerection,pyloerection, vasoconstriction, and other vasoconstriction, and other sympathetic sympathetic

phenomena phenomena

These mechanisms, which in modern terms can be defined These mechanisms, which in modern terms can be defined as as positive sympathetic and motor feedback loopspositive sympathetic and motor feedback loops, are , are fundamental in reffered painfundamental in reffered pain

It is clear that painful stimulation of visceral It is clear that painful stimulation of visceral structures structures

evokes a evokes a visceromuscular reflexvisceromuscular reflex,, so that so that some some

muscles muscles

contract and become a new source of paincontract and become a new source of pain

It has been observed that the It has been observed that the local anesthetic block of the local anesthetic block of the

sympathetic gangliasympathetic ganglia led to the disappearance, or at least to a led to the disappearance, or at least to a

marked marked decrease, of reffered pain, allodynia, hyperalgesia.decrease, of reffered pain, allodynia, hyperalgesia.

In some conditions, In some conditions, reffered somaticreffered somatic pain is long-lasting, pain is long-lasting,

increases progressively, and is accompanied by increases progressively, and is accompanied by

dystrophydystrophy

of somatic structuresof somatic structures. .

Silent myocardial ischemia (SMI)Silent myocardial ischemia (SMI)●● Chest pain is only a late and inconstant marker of episodes Chest pain is only a late and inconstant marker of episodes

ofof

transient transient MI MI in vasospastic angina (30 %), in stablein vasospastic angina (30 %), in stable angina angina

(50 %)(50 %)• Mechanisms ofMechanisms of SMI SMI a) Lack of the pain is, in part, related to thea) Lack of the pain is, in part, related to the duration and severityduration and severity

ofof MI MI. . EpisodesEpisodes shorter than 3 minshorter than 3 min, , and those accompanied by and those accompanied by

aa modest impairment of left ventriclemodest impairment of left ventricle (( in end-diastolic pressure in end-diastolic pressure

inferior to 6 mm Hg) areinferior to 6 mm Hg) are alwaysalways painlesspainless..

Longer and more severeLonger and more severe episodes are acccompaniedepisodes are acccompanied by chest by chest

pain pain in some instances but not in othersin some instances but not in others. .

b) Pacients with predominantly b) Pacients with predominantly SMI SMI appear to haveappear to have a a generalizedgeneralized

defective perception of paindefective perception of pain ((threshold andthreshold and

tolerance).tolerance).

MechanismMechanism: : level of circulating level of circulating -endorphin (?)-endorphin (?)

Disturbances in Disturbances in ppain ain pperception and erception and nnociceptionociception

Most of the disturbances areMost of the disturbances are congenitalcongenital

a)a) Congenital analgesiaCongenital analgesia - - nociceptive stimuli are notnociceptive stimuli are not processed processed

and/or integrated at a level of brain. and/or integrated at a level of brain.

Patient doesPatient does not feel a painnot feel a pain

b) Congenital sensoric neuropathyb) Congenital sensoric neuropathy - - nociceptive stimuli are not nociceptive stimuli are not transmitted bytransmitted by peripheral peripheral nerves ornerves or by spinal afferent by spinal afferent tractstracts..

Acquired disturbancesAcquired disturbances in pain perception and nociceptionin pain perception and nociception

They may occur at They may occur at syringomyelysyringomyely, , disturbances of parietal lobe of disturbances of parietal lobe of

brain, in patients suffering from neuropathy brain, in patients suffering from neuropathy (e.g. chronic diabetes mellitus)(e.g. chronic diabetes mellitus)