Physiological Mechanisms of Pain

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Learning Outcomes
The student will be able to:  Classify pain and understand the physiological processes involved  Appreciate the principles of nociception, inflammation & ischaemia & their role in pain  Understand nociceptive pathways from the periphery to the CNS

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The purpose of pain?



Acute pain:
 

Protection mechanism Damage alert

Chronic pain:
 

Definition? Useful vs Useless pain

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What is Pain?
Pain is an unpleasant sensory and emotional
experience associated with actual or potential tissue damage or described in terms of such damage
( Merksey and Bogduk, 1994)

Pain is a personal experience, depending on culture learning, the meaning of the situation and other factors that are unique to each individual
(Melzack and Wall, 1996)

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Further thoughts ..


The pain of an injury can be excruciating, mentally as well as physically physically

Earvin Magic Johnson
Former National Basketball Association Star

5-13% of patients with sports injuries experience clinically significant levels of emotional distress
(Brewer 1998).

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Pathology = Pain?


Many factors affect normal healing of damaged tissue

Examples? ..

Level of tissue damage not an indicator for pain

 

Compressed NR can be pain free Min. path damage in chronic LBP, WAD


Damaged discs release pro inflammatory chemicals including: growth factors, cytokines and matrix metallo-proteinases, metallooften linked to the pain and mechanomechano-sensitivity
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Current Categorisations for Pain

 

Acute vs Chronic Mechanical vs Inflammatory Causative forces



Label does not always predict outcome, give Rx advice, indicate risk factors etc

WAD, RSI Lateral epicondilytis Headache

Body part
 

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Acute pain
 

 

Acute pain is a short-term shortpain or pain with an easily identifiable cause. Acute pain is the body's warning of present damage to tissue or disease. disease. It is often fast and sharp followed by aching pain. Acute pain is centralised in one area before becoming somewhat spread out. This type of pain often responds well to physiotherapy and medications.
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Chronic Pain


Old definition: definition:



pain lasting 6 months or longer. pain that persists longer than the normal course of time associated with a particular type of injury.

Now defined as: as:



 

This constant or intermittent pain has often outlived its purpose, as it does not purpose, help the body to prevent injury. It is often more difficult to treat than acute pain. Expert care is generally necessary to treat any pain that has become chronic, and coordinated treatment from an interdisciplinary health care team, including medical physicians, physiotherapists, and psychologists or psychiatrists, often beneficial.
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Nociception


The term "pain" is a subjective experience that typically accompanies nociception, but can also arise without any stimulus, stimulus, and thus includes the emotional response. Nociception, on the other hand, is a neurophysiological term and denotes specific activity in nerve pathways. pathways. It is the transmission mechanism for physiological pain. pain.
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Pain Mechanisms
Nociception  Pain from tissues  Afferent nerve endings in tissues excited by stimuli, which can be:
  

Chemical Thermal Mechanical

Butler (2000)

 Cell bodies in DRG only mechano-sensitive part mechanoof a normal nerve root
(Gifford 2001).

Neurotransmitters: Substance P Glutamic acid

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Afferent Nociceptors
A fibres  Large, myelinated  Conduction velocity 6-30 6m/sec  Mechanical & thermal stimuli  transitory pain C fibres  Small, polymodal, unmyelinated, slow  More than A x 2  1% speed of A  Conduction velocity 0.50.51.7 m/sec  Chemical, thermal & mechanical stim.  2o pain
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Dorsal Root Ganglion

   

 

Outside CNS Peripheral NS Brain Afferent cell bodies MechanoMechano-sensitive (unlike NR) ChemicoChemico-sensitive (inflamm.) The Dorsal Root Ganglion is the only mechano-sensitive mechanopart of a normal nerve root ( Gifford 2001).
Crossman & Neary (1998)

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Spinal Cord


Butterfly grey matter

 

DH afferent VH efferent ascending & descending tracts

White matter


Crossman & Neary (1998)

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Dorsal Horn


Substantia gelatinosa tip of DH Laminae I III has collaterals of A & C fibres Enkephalin Sub P release A input (Pain Gate Theory)
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Crossman & Neary (1998)

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A beta sensory afferent fibre

   

 

The largest peripheral nerve fibre Large diameter Myelinated Respond to low stimuli (and are therefore low threshold) such as light touch, pressure and proprioception. Impulses transmitted 30-100m/sec to the CNS 30Normally relate non-noxious mechanical nonLN/PT2023 16

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Ascending Spinal Tracts

Two main tracts for pain 1. Spinothalamic ( anterolateral)
 

Pain info: temp & touch A fibres (Laminae I, V & VIII)

2.

Spinoreticular (anteromedial)
 

Convey late pain messages C fibres (Lamina II VIII)

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Normal response to stimulus

Magnitude of pain Normal

Stimulus Intensity

With injury
Hyperalgesia

1o Hyperalgesia Firing threshold Firing frequency Directly related to area of injury Sensitivity at local site of pain

Magnitude of pain

Normal

Stimulus Intensity

Abnormal response
Allodynia

Magnitude of pain

Normal

Stimulus Intensity

Continued stimulus of nociceptors leads to transmission thru NMDA receptors Impulses pass along spinoreticulothalamic pathways to the corticolimbic system Influx of Ca2+ Mechanisms and changes become interrelated with those involved with chronic pain

Descending Pain Mechanisms



The descending control of pain is manifested via 2 pathways that originate:  midbrain:


periaqueduactal gray (PAG) matter which may in turn project onto (PAG) nucleus raphe magnus (NRM). (NRM).

 

the medulla (rostro ventral medulla):



This nociceptive modulatory system projects to the spinal cord via the dorsalateral funiculus, in which neurons of the funiculus, NRM make inhibitory connections with laminae I, II and V of the dorsal horn. horn. Therefore there is inhibition of the dorsal horn neurons including those of the spinothalamic tract neurons that respond to noxious stimulation.
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Acsending & Descending Paths

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Mechanical Pain


Mechanical pain us. occurs /out inflammation



E.g. slap on the face



Stimulates A fibres (fast, 1o pain) Stimulates A fibres, blocks pain

Rubbing face eases pain



Persistent mechanical stimulus

CNS processing affected Inflammatory processes stimulated

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Inflammation & Nociception



ProPro-inflammatory mediators:
 

Kinins, prostaglandins, H+, K+ and ATP etc Inflammatory Soup

Some directly stimulate nociceptors Some lower the nociceptor thresholds for other inflammatory chemicals
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Degranulation of mast cells Local release of histamine and serotonin ( 5 HT) Neuropeptides released from nerve terminals: substance P and Calcitonin Gene Related Polypeptide ( CGRP)
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SNS & Nociception



Adrenaline, noradrenaline maintain or enhance nociception in inflamed tissues:



effectiveness of chemical mediators Chemical/surgical sympathectomy inflamm. pain & hyperalgesia Adrenaline injection inflamm. pain stress helps to inflamm. pain

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Ischaemia & Nociceptive Pain



Tissue Ischaemia caused by:



Abnormal or sustained postures movement, circulation and tissue fluid

This results in a release of irritant chemicals, acidity due to H+, K+, ATP  Pain results even in Normal tissues
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Catastrophizing

 

Catastrophizing, which is said to be the exaggerated and negative orientation toward pain, may have a role as a mediator to pain Individuals that catastrophise, expect that they cause a new episode of pain or activate an earlier injury. That could create fear of movement and reinforcement of avoidance behaviour. (Buer and Linton, 2002).
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Other terms related to nociception

 

Peripheral sensitisation -The increased excitability of primary afferent nociceptors Central sensitisation - The increased excitability of the spinal cord neurons Windup - low freq repetitive stimulation of C fibres produces grad. in freq discharge until neuron is in a state of continuous discharge. 2Hyperalgesia - hyperalgesia in the uninjured skin surrounding the injury
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Summary
All pain is neurogenic  Stimulus may occur in tissues but pain is regulated by the CNS  Level of pain may not equal extent of tissue damage A little thought. What is your response to patients who say: its all in my head

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References
 

      

Brewer B W. (1998) Psychological applications in clinical sports medicine:Currents status and future directions. Journal of Clinical Psychology in Medical Settings, 5, (1) 91-102. Settings, 91Buer, N and Linton, S .(2002) Fear-avoidance beliefs and catastrophizing: Fearoccurrence and risk factor in back pain and ADL in the general population. Pain, 99, (3), 485-491 Pain, 99, 485Butler, D. (2000) The Sensitive Nervous System. Noigroup Publications. Adelaide Crossman, A.R. & Neary, D. (1998) Neuroanatomy. Churchill Livingstone. Edinburgh Gifford, L. (2001) The Clinical Biology of Aches and Pains- course notes PainsMartin, S B and Knoltzenburg, M (editors) Wall and Melzacks Textbook of Pain, (2006) 5th Edition, Elsevier Rowbotham, D J and Macintyre, P E. (2003) Acute Pain. Arnold, London Shacklock, M. (2005) Clinical Neurodynamics. Elsevier. Edinburgh Wall, P (1999) Pain: the science of suffering. Phoenix. London
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Useful Websites
 

achesandpainsonline.com iaspiasp-pain.org

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