Physiological Effects Of Manual Therapy Flashcards

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1
Q

What components are part of the corticolimbic system?

A
  • amygdala => fear + anxiety emotions (nuclei)
  • hippocampus => memory + reward/motivation
  • hypothalamus => maintains homeostasis
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2
Q

What happens in the theoretical model of pain onset?

A
  • 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
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3
Q

What is the aim of manual therapy when treating a patient in pain?

A
  • to raise the lowered pain threshold to a ‘robust’ pain threshold
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4
Q

What are the goals of pharmacological pain treatment?

A
  • increase inhibitory neurotransmitter => analgesia => removing response between Nociception + pain
  • prevent peripheral + central sensitisation
  • restore normal responsiveness of Nociception
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5
Q

How is pain modulated in the amygdala?

A
  • thoughts
  • beliefs
  • expectations
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6
Q

Which drugs affect the midbrain/PAG?

A
  • opioids
  • NSAIDs
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7
Q

Which drugs affect the medulla?

A
  • opioids
  • cannabinoids
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8
Q

Which drugs affect the dorsal horn?

A
  • tricyclic anti-depressants (TCAs)
  • selective serotonin/noradrenaline reuptake inhibitors (SSRIs or SNRIs)
  • alpha-2 agonists
  • opioids
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9
Q

What are the side effects of common pain killers?

A
  • 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
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10
Q

What are the effects of STM?

A
  • 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)
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11
Q

What happens during joint articulation?

A
  • 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)
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12
Q

What effect does spinal manipulation have on pain?

A
  • 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
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13
Q

What are the effects of manual therapy on the autonomic NS?

A
  • 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
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14
Q

What is the role of light touch (c-fibres) in pain reduction?

A
  • 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
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15
Q

What are the peripheral tissue drivers of pain in the nervous system (neural axis)?

A
  • 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
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16
Q

What are the peripheral tissue drivers of pain in the spinal cord (neural axis)?

A
  • 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
17
Q

What are the peripheral tissue drivers of pain in the brain stem (neural axis)?

A
  • altered biological patterns e.g. sleep, breathing, hormone release
  • heightened state of arousal + stress
  • dismissed pleasure from altruistic acts, feeding etc.
18
Q

What are the peripheral tissue drivers of pain in the limbic system (neural axis)?

A
  • depression + psycho-emotional states
  • anxiety + fear
  • inappropriate retained memory of trauma
19
Q

What are the peripheral tissue drivers of pain in the neo-cortex brain platform (neural axis)?

A
  • 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
20
Q

What mechanisms of pain relief are available at the distal neuroaxis

A
  • 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)
21
Q

What mechanisms of pain relief are available at the proximal neuroaxis?

A
  • 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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22
Q

What central mediators can impact pain experience?

A
  • 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
23
Q

What peripheral mediators can impact pain experience?

A
  • Biomechanical e.g. increase ROM + decrease passive stiffness + active stiffness
  • neurophysiological e.g. change concentration of inflammatory + pain mediator substances
24
Q

How can a patient be treated ‘bottom-up’ for pain?

A
  • manual therapy
25
Q

What are ‘top down’ moderators of pain?

A
  • habituation
  • graded exposure to mechanical stimuli
  • sensory discriminions training
  • cognitions
  • expectations
  • placebo/meaning response
  • contextual factors
  • therapist effect
26
Q

What is the effect of attention + distraction on pain?

A
  • distraction + hypnotic => attenuation of pain
  • anticipation + focus => exacerbation of pain
27
Q

What is habituation?

A
  • 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
28
Q

How

A