Pain, Neuromuscular Control and Biofeedback

Nociceptive pain

somatic or visceral

Neuropathic pain

peripheral or central

Kubler-Ross Death and Dying Model

1.) 5 stages of response to terminal illness → denial, anger, bargaining, depression and acceptance 

2.) applicability to athletic injury is not good 

Cognitive Appraisal model

1.) response to injury depends on understanding of the injury 

2.) response to injury is not neatly divided into stages in particular order → some get angry, others not

3.) response to injury can be influenced by the actions and message of the doctor 

Ability to cope with injury is influenced by

1.) family, friends, co-workers, team-mates, stress levels

2.) knowledge and understanding alter the response

3.) find the right level → don’t oversimplify but don’t overwhelm

Pain

1.) warns of impending injury, essential for survival

2.) protects the body and signifies something is wrong

3.) limit further injury 

Reducing pain

1.) facilitates the return to normal movement and function

2.) limits adaptive changes that may contribute to subluxation and hinder long term subluxation correction

Chiropractors reduce pain by

1.) removing subluxations

2.) using EPAs → pain reduction to enable patient to start therapeutic exercise, reduce pain to avoid subclinical adaptations that can lead to subluxation patterns and long term patients

Transmission of pain

1.) most common use of therapeutic modalities is to reduce pain levels

2.) alter neural input to brain where pain perception and response occur 

3.) can occur at the periphery, spinal level, ascending pathway, supraspinal level, or descending pathway 

Peripheral sensory receptors

1.) special, visceral, superficial and deep

2.) special: sight, taste, smell, hearing and balance 

3.) visceral: hunger, nausea, distension, visceral pain 

Transduction

1.) process of changing energy of nociception into electrical action potential in the neuron 

2.) nociceptors normally have high threshold 

meissner corpuscles 

pressure and touch 

merkle cells

skin stretch / pressure

thermoreceptors

hot and cold receptors → temperature change

Golgi tendon organs

change in muscle length and spindle tension

pacinian corpuscles

change in joint position and vibration 

ruffini endings 

joint end range, possible heat 

nociceptors

free nerve endings → pain

Peripheral transmission: first order transmission

1.) peripheral nerve fiber, cell body in dorsal root ganglia and synapse in the spinal cord

2.) typed according to structural and functional characteristics → diameter or nerve, degree of myelination, function of nerve

A-beta fibers

1.) large

2.) fast transmission 

A-delta

1.) smaller

2.) slower transmission

First order afferents: A-beta fibers

1.) hair follicles, Meissner corpuscles, pacinian corpuscles, merkle cells, ruffini endings

2.) touch, vibration, and hair deflection,

3.) large diameter and myelinated → fast conduction velocity 36-72 microseconds, low threshold

First Order Afferents: A-delta fibers

1.) warm and cold receptors, hair follicles, free nerve endings

2.) touch, pressure, temperature and pain 

3.) free nerve endings respond to noxious stimuli such as pricking, pinching and crushing 

4.) myelinated, smaller diameter than A-beta, slower conduction velocity 

C fibers

1.) pain, touch, pressure, temperature (Found in skin)

2.) Pain (in muscle) → include efferent postganglionic fibers of sympathetic nervous system, mechanoreceptors, nociceptors, and thermoreceptors

3.) smallest peripheral nerves associated with pain → un-myelinated, small diameter, slow conduction velocity

Central transmission

1.) 1st order neurons synapse in the spinal cord dorsal horn → cell body of the 2nd order neuron (T-cell) is in the dorsal cell 

2.) multiple tracts carry information through spinal cord to the brain → cell bodies of the 3rd order neurons are located in the thalamus in various cluster of nuclei 

3.) VPL and VPM are most important parts of the thalamus for pain transmission 

VPL

ascending pain fibers from the body synapse

VPM

fibers from the head and face synapse

Thalamus

1.) modulates input and transmission to the somatosensory cortex → localized and discrimination occur in the postcentral gyrus

2.) Relays to the limbic system → regulates emotional, autonomic and endocrine response to pain (affected motivational component) 

Modulation phase: any activity after the cortex has received input 

1.) have an excitatory or inhibitory role on new impulses → hypothalamus, pituitary, reticular formation, raphe nucleus

2.) when these are not inhibited can lead to affective emotional response similar to shock 

3.) network of messages and activation of brain centers may exacerbate the painful event and lead to windup 

Peripheral pain modulation: pain modulation targeted at desensitizing of peripheral nociceptors

1.) increases threshold → more difficult to stimulate, fewer pain impulses transmitted to spinal cord

2.) may try to decrease the effects of chemical mediators in the inflammatory process

Gate theory

1.) non-painful stimulus can block the transmission of noxious stimuli → substantia gelatinosa in dorsal horn of spinal cord acts as switch operator

2.) interneuron that utilizes enkephalin is present in substanstia gelatinosa → inhibits pain transmission at the dorsal horn

Central pain modulation

1.) pain transmission occurs through a complicated network of interneurons

2.) activate numerous structures, balance between alerting the patient that something is dreadfully wrong and calming then so they can’t solve the problem 

Motor pain modulation

1.) low frequency, high intensity stimulation of peripheral nerves (motor TENS)

2.) causes activation of reticular formation and pituitary gland, descending endogenous opiate system 

3.) inhibitory effect on lower pain pathways, descending pain modulation (analgesia) 

Noxious Pain modulation 

1.) Electrical stimulation of C fibers in the injury area (Noxious TENS) 

2.) activates periaqueductal gray and the raphe nucleus 

3.) serotonin neurons in the dorsal horn inhibit the second order neuron either directly or through an interneuron

4.) also with ice stimulation of C fibers during burning and aching sensation

Exercise induced Hypoalgesia

1.) decreased pain sensation during physical activity

2.) increased endogenous opioids and catecholamines during exercise

3.) intensity ~70% VO2 max. Also seen to lesser degree with anaerobic exercise

Neuromuscular control consists of 3 components all of which must be addressed in a rehabilitation plan

consciously controlled muscle contraction, reflex response, complex movement patterns

Conscious Muscle contraction 

quick and efficient voluntary contractions are desired, injury can lead to inhibition of mm contraction 

Reflex Responses

1.) damage to ligaments, capsule, tendons

2.) interrupts or decrease the afferent signals = loss of proprioception

3.) difficulty to reflexively contract mm to control balance

Complex movement patterns

1.) unconscious movement patterns, these “take over” after practicing an activity

2.) injury leads to loss of these unconscious patterns

swelling

1.) stretch receptors in the joint capsule of the knee

2.) with joint effusion send signals to CNS, causes reflex inhibition to vastus medialis

3.) 200ml in the ankle inhibits fibularis muscle group

When active exercise is painful 

the motor patterns change which perpetuates abnormal motor control and slows recovery possibly leading to further injury 

Altered nervous system input

1.) damage to ligaments, capsules, tendons → alters mechanoreceptor and neuromuscular control of joints

2.) shown to have been affected with injury → balance, protective reflexes, force output, joint stability, position sense

Restoring neuromuscular control

1.) active rehab → EPAs to permit pain free exercises

2.) neuromuscular electrical stimulation for muscle activation

3.) EMG feedback for retraining

Biofeedback

1.) use of information to bring physiological events to conscious awareness in the patient 

2.) clinician, mirror, video tape, patient, electromyography 

3.) measuring stress, useful in stress relief and stress management 

Electromyographic biofeedback

1.) teaching aid, electrical activity in the muscles detected → visual or auditory feedback

2.) relearning motor patterns and motor control, relaxation of muscle spasm and muscle guarding 

Surface or needle electrodes 

needles = specific portion of muscle

surface = whole muscles or muscle groups

Clinical applications

1.) inhibited muscles from injury etc → EMG provides positive feedback

2.) helps reduce trial and error, helps reduce patient frustration

3.) if unable to generate any contraction → tap or stroke the muscle, neuromuscular stimulation (Russian stim) 

Functional progression

1.) adjusting EPAs, active care

2.) reduce pain and prevent/minimize adaptions

3.) early restoration or neuromuscular control starts with single muscles but must progress to specific activities