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Changes in Nueromotor Control With Pain

Psych 376 - Group Project

bob frank

on 10 April 2014

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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.
Athrogenous inhibition

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

Brain MRI

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.

Fibromyalgia Pathway

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
Multidimensional Disorder
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

Arthritis Pain

Which of the following is NOT a characterization of fibromyalgia?
a. Body stiffness
b. Chronic musculoskeletal pain
c. Increased pain sensitivity
d. Sleep disturbances

Clicker Question

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
Four Types:
1. Mechanical/tactile
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
Pain matrix

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

Neuro-physiological Model
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
Psychosocial Model
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
Trigger points

Types of Pain

Akathic Discomfort


Central Pain Syndrome


Why is Pain Important

- Awareness

- Protection

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!
Pain Mechanisms

(0.00- 2:00)

Rest Tremor
Stooped Posture
Focal Dystonia
Postural Instability

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
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