Physiological Effects Of Manual Therapy Flashcards
What components are part of the corticolimbic system?
- amygdala => fear + anxiety emotions (nuclei)
- hippocampus => memory + reward/motivation
- hypothalamus => maintains homeostasis
What happens in the theoretical model of pain onset?
- mechanical irritation/inflammation starts => below corticolimbic pain threshold
- over time mechanical/inflammation continues => above corticolimbic lowered pain threshold
- get a ‘sudden’ acute onset of pain => hyperalgesia => pain goes above ‘robust’ pain threshold
- however, could be building over time, prior to threshold is ‘under the radar’’
- nociceptive is over the corticolimbic threshold
- corticolimbic = limbic + amygdala => descending and only stimulated when threshold is crossed
- thresholds aren’t fixed; based on past history and experience
What is the aim of manual therapy when treating a patient in pain?
- to raise the lowered pain threshold to a ‘robust’ pain threshold
What are the goals of pharmacological pain treatment?
- increase inhibitory neurotransmitter => analgesia => removing response between Nociception + pain
- prevent peripheral + central sensitisation
- restore normal responsiveness of Nociception
How is pain modulated in the amygdala?
- thoughts
- beliefs
- expectations
Which drugs affect the midbrain/PAG?
- opioids
- NSAIDs
Which drugs affect the medulla?
- opioids
- cannabinoids
Which drugs affect the dorsal horn?
- tricyclic anti-depressants (TCAs)
- selective serotonin/noradrenaline reuptake inhibitors (SSRIs or SNRIs)
- alpha-2 agonists
- opioids
What are the side effects of common pain killers?
- paracetamol = liver damage
- NSAIDS = gastritis, ulcers, kidney failure, stroke
- codeine - constipation
- morphine - addiction, severe constipation, teeth fall out
- amitriptyline - dry mouth => suicidal tendencies
- gabapentin - dizziness, somnolence (drowsiness), peripheral oedema
- NMDA - receptor antagonists e.g. katamin
- cannabinoids
- capsaicin patches
What are the effects of STM?
- depth of technique will cause different neurophysiological response
- activation of a-beta fibres => pain-gating where c-fibre input is abolished
- deeper techniques => mildly noxious => conditioned pain modulation => activating descending PAG-RVM pathway
- painful stimulation => DNIC (diffuse noxious inhibitory control)
What happens during joint articulation?
- stretching joints -> intra-articular pressure + lengthen capsules + ligaments => reduced afferent barrage (input signal reduced)
- increases pressure-pain thresholds (PPT) locally + widespread
- no effect on thermal pain thresholds (TPT)
What effect does spinal manipulation have on pain?
- changes secondary hyperalgesia + allodynia
- changes pressure pain threshold
- changes suprathreshold heat response
- changes temporal summation threshold (signal sent to axon hillock doesn’t reach threshold to send afferent signal to brain)
- perceived pain intensity
- perceived pain threshold on ipsilateral + contralateral side increase following SMT
- remote + local changes
What are the effects of manual therapy on the autonomic NS?
- HVT + articulation => increase HR + skin conductance + decrease in salivary amylase (increased sympathetic activity)
- balance ligamentus techniques, crank-sacral => altered parasympathetic activity
- SMT => increase in sympathetic + decrease in parasympathetic activity
What is the role of light touch (c-fibres) in pain reduction?
- stroking, warmth + light pressure => oxytocin + opioid release (pag+rvm)
- promotes relaxation + well-being
- c-tactile afferents on non-hairy skin => project to insular cortex
- forms an affective homunculus in insular cortex => map of pleasure
What are the peripheral tissue drivers of pain in the nervous system (neural axis)?
- pro-inflammatory chemicals from tissue damage or neurogenic inflammation
- active immune response + chemical accumulation
- build up of metabolic waste
- inappropriate mechanical response from tissues
- direct irritation of a nerve
What are the peripheral tissue drivers of pain in the spinal cord (neural axis)?
- spinal cord c-fibre nociceptive input (neurogenic inflammation => knock on effect)
- reduced disinhibition
- abnormal activity in inter-neurone => referred pain
- physiological + pathological lowering of depolarisation of potentials
What are the peripheral tissue drivers of pain in the brain stem (neural axis)?
- altered biological patterns e.g. sleep, breathing, hormone release
- heightened state of arousal + stress
- dismissed pleasure from altruistic acts, feeding etc.
What are the peripheral tissue drivers of pain in the limbic system (neural axis)?
- depression + psycho-emotional states
- anxiety + fear
- inappropriate retained memory of trauma
What are the peripheral tissue drivers of pain in the neo-cortex brain platform (neural axis)?
- belief constructs e.g. hurt = harm
- no context of pain experience
- explaination of pain reduces sense of understanding/control
- reduced inhibition + loss of discreetness in somatosensory cortex (smudging)
- inappropriate motor programs
- excessive prediction of pain
What mechanisms of pain relief are available at the distal neuroaxis
- reduce local tissue afferent input
- increase safe afferent (non-noxious) input
- gate control
- increase descending inhibition (DNICs + endogenous analgesia)
- increase c-fibre afferent input to insular (light touch)
What mechanisms of pain relief are available at the proximal neuroaxis?
- distraction
- habituation
- removal of painful movement memories
- learn pain-free movement memories
- pain education/cognitive therapies
- graded exposure to mechanical stimuli
- set expectations
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What central mediators can impact pain experience?
- changes in spinal excitability + motor function
- decrease in cortical excitability + activation in brain pain processing areas
- decreased activation of facilitatory in inhibitory pathways
- changes in resting state bran functional connectivity
What peripheral mediators can impact pain experience?
- Biomechanical e.g. increase ROM + decrease passive stiffness + active stiffness
- neurophysiological e.g. change concentration of inflammatory + pain mediator substances
How can a patient be treated ‘bottom-up’ for pain?
- manual therapy
What are ‘top down’ moderators of pain?
- habituation
- graded exposure to mechanical stimuli
- sensory discriminions training
- cognitions
- expectations
- placebo/meaning response
- contextual factors
- therapist effect
What is the effect of attention + distraction on pain?
- distraction + hypnotic => attenuation of pain
- anticipation + focus => exacerbation of pain
What is habituation?
- a type of synaptic learning => decreased behavioural responses to repeated stimulation
- decreased neurotransmitter => progressive decrease in size of postsynaptic potential
- MT sensory input => completes with pain => restore sensitive nervous system
- reorganisation of cortical map
- non-threatening stimuli should habituate; otherwise they are a threat + sensitise
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