Pain Pathways Dr Sameer Gupta Consultant in Anaesthesia and Pain Management, NGH
Objective To give you a simplistic and basic concepts of pain pathways to help understand the complex issue of pain
Pain Definition Unpleasant SENSORY and EMOTIONAL experience associated with actual or potential tissue damage
Pain Is having pain Any good? Evolutionary process.
Physiological Effects of acute pain Positive role: warning of tissue damage immobilization for healing protection of the species: establishment of memory
Pain Physiological responses Affect HR, BP, RR, GIT Learned Behaviour response Memory
Classification of Pain Acute Pain : Post operative Pain, non surgical cause Cancer Pain :Palliative Care Chronic Non Cancer Pain Visceral Pain Musculoskeletal pain
Classification of Pain Nociceptive: inflammatory Neuropathic: nerve related Mixed
First attempts (cancer pain)
Acute Pain Generally last less than a week Results from activation of sensory nerve fibres called nociceptors
Pain Pathways (nociceptors) Myelinated A delta Fibres Unmeyelinated C afferent fibres Location: most body tissues except brain, liver
Pain Experience of pain is a complex mix of activation of different afferent fibre types Eg A-beta fibres
First attempts 1664 Descartes, Pain a specific sensation
Pain Pathway Stimulus Nociceptors Spinal Cord, Modulation happens Experience, learned behaviour Memory Perception Brain
Alternatively Sensors and conduction: Stimulus and nociceptive receptors Central Processing and modulation: Spinal cord and Brain Effectors: behaviour, reaction, emotions
Stimulus Noxious Stimulus Mechanical Thermal chemical
Tissue Injury Break down of membrane lipids Phospolipase A2 Arachidonic Acid Cyclooxygenase (Cox) Prostaglandins
Products of Arachidonic Acids Act directly on the nociceptors ( peripheral terminals of Aδ and c fibre) and lower their threshold to thermal stimuli. Results: a sensation of burning at room temperature
Nerve Fibres Transmitting Pain C Fibres: unmyelinated fibres, Characterised by diffuse dull intense pain A Delta Fibres: small myelinated fibres conduct localised sharp sensation
Cortical Areas Somatosensory cortex Prefrontal cortex Thalamus PAG Ascending pathw ay Excitatory Neurotransmitters Eg Glutamate Noxious Stimulus
At the level of spinal cord
Experience of pain
Wind Up (Central Facilitation) Poorly understood,? Clinical relevance in pain Mediated via C fibres Repeated frequency dependent stimulation ( usually electrical stimulus) results in increase in amplitude of the neurons in the spinal cord. Possibly a role of NMDA receptors and substance P May result in central sensitisation
Are there any safeguards or protection? Mechanisms Descending Pathways Gate control Theory
Past experiences, Mood, Memory, other sensory inputs Central Processing Descending pathways Modulation Ascending pathw ay Excitatory Neurotransmitters Eg Glutamate Noxious Stimulus
Gate control theory Balance of activity between large and small fibres Interneurons of the substansia gelatinosa regulate the input in Lamina V
Gate control theory
Gate control Theory Aβ Fibres Dorsal Horn Spinal Cord Brain Nociceptive Stimulus
Gate control Theory Aβ Fibres Dorsal Horn Spinal Cord Brain Nociceptive Stimulus
What does that mean? Low intensity stimulation of the skin or peripheral nerves or vibration will generate analgesia
Is there any practical application of this theory Rubbing, application of heat, counter irritation creams TENS ( trans cutaneous nerve stimulation) Spinal Cord Stimulation Possibly Acupuncture
Descending Pathways Modulation of gate control are influenced by Higher Centre inputs Higher centre inputs are modulated by various neurotransmitters
Past experiences, Mood, Memory, other sensory inputs Central Processing Descending pathways Modulation Ascending pathw ay Excitatory Neurotransmitters Eg Glutamate Noxious Stimulus
Endogenous Pain Control System Role of Higher Centres Peri Aque-ductal Grey, Locus Cerulus Key role Inhibits the firing of the dorsal horn neuron that respond to noxious stimulus (gate control theory). Changing the levels of neurotransmitters at the level of synapses
Basis of Pharmacological treatment of some pain Reducing Excitatory Neurotransmitters and excitation of the nerve (with respect to pain transmission) Basis for using anti epileptics, Local Anaesthetics (Na channel blockade) Enhancing Inhibitory Neurotransmitters Noradrenaline and Serotonin Basis for using Anti depressants
Endogenous Pain Control System Opioids Receptors High concentrations of Opioid receptors in Spinal cord and Brain Body produce endogenous opioids
Endogenous opioids peptides Enkephalin Dynorphine Beta endorphine: effects similar to morphine
endorphines Released in the presence of pain Practical utilities 1) acupuncture: bearable pain 2) Placebo 3) Psychological modulation of pain
knowing pathway helped in controlling pain?
Medication Prostaglandins act directly on the nociceptors reduces there threshold and normal stimuli can activate these producing a sensation of pain (peripheral sensitization) NSAIDS and possibly Paracetamol utitlises this
Medications Opioids: morphine Local anaesthetic: block conduction of the nerve
Definition Chronic Pain Ongoing persistent pain greater than 3-6 months pain experience persists beyond the usual course of an acute disease or after healing/cure has taken place or recurs at intervals for months or years or due to persisting stimulation in areas of ongoing tissue damage
Chronic Pain serves no useful biological function, but has profound effects on the patient and their family Physical : Immobility Emotional: distress social : little social interaction/ isolation economical : job issues Day to day activity is severely affected.
Pain presentation
Treatment consist of therapies aimed at all these areas and not focused to one particular area
Chronic Pain Principles of Treatment Improve Pain Perception Improve Function / Mobility Improve Sleep Improve Emotional and Psychological Consequences of Pain IMPROVE QUALITY OF LIFE