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Changes in Nueromotor Control With Pain
Transcript of Changes in Nueromotor Control With Pain
As many as half of all PD patients experience pain related to the disease
Some patients pain becomes so severe, other symptoms become overshadowed
5 general categories of pain
Pain can be managed by gaining more control over ones disease
Pain and PD
True/False: The Frontal brain areas remain unaffected in CLBP patients
Arthritis pain yields new motor unit recruitment strategies that aim to minimize pain and maintain homeostasis
Decreased agonist activation and slight increased antagonist activation
Theorized model- phasic modulation of excitatory and inhibitory interneurons supplied by high-threshold sensory afferents.
Pain Adaption Model
Mechanoreceptors in articular cartilage have a large influence on movement, in osteoarthritis the afferent information from the articular areas can be altered
Arthritic joint pain can also cause muscle inhibition in the ipsilateral limb due to reduced motor neuron excitability
In addition proprioceptive impairment from the affected articular area to the supraspinal centers slows centrally driven muscle activity of the afflicted joint
Arthritis and Motor Control
Gray matter decrease observed in chronic pain vs. pain free
Why would it decrease?
Lack of noxious input leads to decrease in gray matter.
This means the constant pain is caused by brain itself, not a stimulus
The pain is often worsened with movement
Pain causes a reluctance in movement.
Fear of activity leads to deconditioning
The lack of movement can lead to more emotional disturbances for those affected.
Fibromyalgia and Motor
Golgi tendon and muscle spindle involvement
Neurons involved have been sensitized by previous painful experience.
Causes a reflexive avoidance behavior, occurring before the pain is felt.
Chronic condition involving muscle fatigue and significant pain in the muscles, tendons and ligaments
Involves inflammation, but differs from arthritis because it does not involve inflamed joints nor cause joint deformities.
The chronic pain is associated with sleep disorders, depressed mood, cognitive impairment and fatigue.
SI, SII, insula, and ipsilateral cerebellum are activated in response to allodynia
Prefrontal and SII cortices activation in response to heat/pain
Allodynia has stronger activation of bilateral SII, ipsilateral cerebral cortex, bilateral prefrontal cortex, BG, and contralateral cerebellum (compared to norm pain)
Pathology of Allodynia
1. Specific Theory:
Body has a separate system for pain
2. Pattern Theory:
Pain receptors shared with other sensory systems
From high levels of neural activity as a result of intense stimuli
3. Gate Control Theory
Large fibers create “gate” in spinal cord
Gate opens/closes depending on activity in pain fibers and peripheral fibers, and descending messages from brain
More pain more small fibers open gate
Theories Of Pain
Most commonly seen
Impairment or deficits in the primary direction of pain
Patients adopt postures and movement patters that stress the pain sensitive tissues
Mal adaptive motor control behavior provides an ongoing mechanism for tissue strain and peripheral nociceptive drive
Control Impairment Classification
High level of disability, altered central pain processing, amplified non remitting pain.
Disordered movement and motor control impairments
Present with psychosocial features including pathological anxiety, fear, anger, depression, poor coping strategies
Lack of clear and consistent mechanical provocation or relieving patterns
Treatment of the whole person
Exits where mal adaptive movement or control impairments are associated with poor coping strategies that result in chronic abnormal tissue loading
Excessive or reduced spinal stability
Movement impairments are characterized by pain avoidance behavior act as the underlying mechanism that drives the pain
Chronic Pain Derived From the Forebrain
Acute Pain is a symptom of an injured tissue
Herniated Disc- Once the pressure on the nerve is alleviated, the pain diminishes
Pain as a protective reflex- limiting movement until pain subsides
Chronic Pain persists longer than the normal tissue healing time; more than 3-6 months
Influences other than damaged tissue needs to be addressed
Need to classify the disorder based on the mechanisms that -DRIVE the pain
Lack of control, lifelong pain
Specific:15% of cases
Non-specific: 85% of cases-tissue sprains and strains not resolved beyond normal tissue time
Acute vs. Chronic Pain
Inhibition of voluntary and reflexive motor neuron output causes muscle weakening over time
Reduced excitability of quadriceps in knee OA patients has shown to diminish proprioceptive acuity
In addition arthrogenic impairment decreased postural stability and is associated with reduced functional performance
Pain Adaption Issues
Joint inflammation causes peripheral sensitization and central sensitization
Sensitization influences afferent and efferent neuronal processes
Which of the following is NOT a characterization of fibromyalgia?
a. Body stiffness
b. Chronic musculoskeletal pain
c. Increased pain sensitivity
d. Sleep disturbances
Imagination of allodynia leads to increased activation of anterior cingulate cortex, bilateral SII, insular cortex, and prefrontal cortex
Allodynia-experienced patients activated contralateral thalamus, anterior cingulate, amygdala, SI, SII, insular and prefrontal cortices
Allodynia in-experienced only activated contralateral SI and bilateral SII
Neural Changes with Allodynia
Medial thalamic pathway to fontal lobe
Nociceptive cells and mechanoreceptors originate in dorsal root ganglia
Nociceptive tract crosses to contralateral spinal cord
Mechanoreceptors cross at lower medulla level
Allodynia pathway synapses and ends in the somatosensory cortex
Pathology of Allodynia
Defined as pain due to a normally non-noxious stimulus
Cause = unknown, possibly spinal cord injury, re-organization of nociceptors and mechanoreceptors
2. Static mechanical - pain in response to light touch/pressure
3. Dynamic mechanical - pain in response to brushing
4. Thermal (hot or cold) - pain from normally mild skin temperatures
VR1 receptor converts noxious energy into action potential
Afferents synapse on lamina I and II and continue along the spinothalamic tract
A- fiber nociceptors vs. C – fiber nociceptors
Mechanisms Of Pain
Young group (50-69) vs Old group (70+)
Early vs. Advanced PD
Present with a painful loss or impairment of normal physiological movement
Movement related to fear and anxiety associated with pain reinforces the poor coping strategies and enhances muscle guarding.
Mal adaptive response to the pain disorder as the compensations for the pain in turns becomes the mechanisms that drive it.
Restore normal movement by reducing fear
Movement Impairment Classification
Forebrain Facilitation of Pain
Nervous system undergo changes to its cortical mapping and processes of pain memory
Pre-sensitized to the exacerbation and recurrence of pain
Mal adaptive coping strategies
Zusman research positive factors have descending inhibitory effect on pain via the forebrain
Woby 2004 cognitive behavioral interventions are effective in reducing disability in specific groups with non specific CLBP
Motor Control Model
Movement and motor control impairments occur second to the presence of pain
Following an acute low back injury, ongoing mal adaptive motor control behavior provides a basis for on going peripherally driven nociceptors sensation leading to a chronic pain state.
Chronic Low Back Pain
Causes and Symptoms
No known root cause to Fibromyalgia, but can be seen after an injury
Pain is amplified due to disordered regulation of central processing
Increased substance P in spinal cord
Low levels of blood flow to the thalamus
Low levels of serotonin and tryptophan
Types of Pain
Central Pain Syndrome
Why is Pain Important
4. When diagnosed, a healthcare professional should be just as concerned with the patients emotional state, as they should be with the patients physical condition.
3. Pain can be reduced with the proper treatment.
2. If a patient diagnosed with PD has musculoskeletal pain, they also have radicular-neuropathic pain.
1. Everyone experiences pain directly related to having Parkinson’s.
True or False!
Review of Parkinson’s Disease
- As many as half of all PD patients experience pain related to the disease
- Some patients pain becomes so severe, other symptoms become overshadowed
- 5 general categories of pain
- Pain can be managed by gaining more control over ones disease
By Alex Linde, Kasey Flynn,
Jasmine Braman, J.P. Benoit,
& Mallory Hillman
Just recently has pain been recognized as being a symptom related to PD
Muscular and peripheral neuropathic pain types associated with lower pain threshold, lower pain tolerance, and lower heat thermode
Different types of pain arise from abnormal nociceptive input processing at various levels of the CNS
Only mild-changes in pain-processing mechanisms related to PD
Primarily dopamine leading to abnormal pain processing
Although evidence also supports other neurotransmitters may also contribute
Similar pain ratings
Both most commonly reported musculoskeletal pain
Older group reported slightly more radicular-neuropathic pain