ΒΆ Movement neglect
Merged from 2 sources β review for redundancy.
ΒΆ From immunology/
ΒΆ Definition
Movement neglect is a learned neurocognitive phenomenon where the brain progressively withdraws motor control and sensory processing from a body part or movement pattern following pain or injury, resulting in cortical reorganization that persists even after tissue healing. This represents a maladaptive protective strategy driven by fear-avoidance pathways, where the threat value of movement becomes encoded in the pain matrix, creating a self-perpetuating cycle of reduced motor output, sensory smudging, and pain expectation. Unlike hemispatial neglect following stroke, movement neglect occurs in chronic pain conditions without obvious structural brain injury but produces measurable cortical shrinkage and sensory discrimination deficits.
ΒΆ Picture It
Imagine your brain maintains a detailed city map for every body part β a precise district with clear streets, landmarks, and traffic patterns representing motor control and sensory feedback. When your shoulder gets injured, the brain throws up roadblocks: "DANGER β shoulder movement ahead." Initially protective, this makes sense while tissues heal. But here's the problem: even after the physical roadblocks (tissue damage) are removed, the warning signs stay up. The city planners (motor cortex) stop investing in that district. Streets get narrow and vague. The traffic control center (basal ganglia) reroutes everything around the "dangerous" shoulder district. Maps become outdated β you can't tell left shoulder from right on a quiz (laterality recognition fails). The fire department (pain matrix) now responds to any mention of shoulder movement, even when there's no actual fire. Meanwhile, the neglected district deteriorates from disuse β buildings (muscles) shrink, pipes (fascia) get clogged, joints rust. Now when you finally try to use that route, it genuinely hurts because the infrastructure has degraded. The brain says "See? I told you it was dangerous" β and the cycle deepens. The shoulder becomes a ghost district on your brain's map.
ΒΆ Mechanism
Movement neglect develops through a cascading neurocognitive process involving fear learning, cortical reorganization, and tissue adaptation:
Phase 1 β Initial Pain and Threat Learning
- Nociceptive input from injured tissue (mechanical, inflammatory) β A-delta and C fibers β dorsal horn
- Ascending pain signals β spinothalamic tract β thalamus β anterior cingulate cortex (ACC) and Amygdala
- ACC processes pain unpleasantness and threat value β activates fear network (amygdala, ACC, insula)
- Amygdala encodes emotional memory: "shoulder movement = threat" β strengthens via long-term potentiation (LTP)
- Prefrontal cortex (PFC) fails to downregulate amygdala (reduced top-down inhibition in chronic pain)
Phase 2 β Cortical Reorganization (Motor Smudging)
- Reduced movement β decreased input from proprioceptors and mechanoreceptors
- Primary motor cortex (M1) representation of neglected limb shrinks (30-50% reduction in cortical territory)
- Adjacent body part representations expand into neglected territory (maladaptive plasticity)
- Precision of motor commands deteriorates β movements become less coordinated when attempted
- Premotor cortex and supplementary motor area reduce activity for neglected limb movements
Phase 3 β Sensory Discrimination Decline
- Reduced tactile and proprioceptive input β primary somatosensory cortex (S1) reorganization
- Two-point discrimination threshold increases (20-50mm worse than unaffected side)
- Sensory cortical maps become "smudged" β overlapping, imprecise representations
- Laterality recognition slows (200-500ms delay) β can't quickly identify left vs right image of neglected limb
- Body schema in posterior parietal cortex becomes outdated
Phase 4 β Motor Program Habituation
- Protective muscle guarding becomes encoded in basal ganglia motor programs
- Habitual avoidance patterns β dorsolateral striatum (habit learning)
- Compensatory movement strategies become automatic (using trunk instead of shoulder)
- Cerebellum adapts to altered movement patterns, reinforcing compensation
Phase 5 β Learned Pain (Central Sensitization Component)
- Movement intention alone activates pain matrix: ACC, insula, S1, prefrontal cortex
- Pain expectation β periaqueductal gray (PAG) fails to activate descending inhibition
- May involve increased rostral ventromedial medulla (RVM) facilitation β enhanced spinal nociception
- NMDA receptor upregulation in dorsal horn β wind-up and central sensitization
- Pain becomes uncoupled from actual tissue damage (nociceptive-independent pain)
Phase 6 β Peripheral Tissue Changes (Secondary Pathology)
- Disuse β muscle atrophy (muscle protein synthesis < breakdown)
- Joint capsule fibrosis β adhesions, reduced range of motion
- Fascial adhesions β Thoracolumbar Fascia (TLF) Innervation changes, mechanoreceptor dysfunction
- Reduced blood flow β tissue hypoxia, metabolic dysfunction
- These real tissue limitations create genuine movement restriction and pain on movement
Phase 7 β Positive Feedback Loop
Less movement β more cortical smudging + tissue degradation β more pain on attempted movement β reinforced threat memory β even less movement
Neurotransmitter/Neuromodulator Changes:
- Dopamine signaling in reward pathways altered (movement becomes less rewarding)
- GABA inhibition may be reduced in motor cortex (reduced intracortical inhibition)
- Glutamate excess in pain pathways (excitotoxicity potential)
- BDNF expression reduced in motor cortex with disuse
- Endogenous opioid system may show altered receptor density (tolerance or upregulation)
ΒΆ Clinical Significance
Movement neglect is critically important in cPNI practice because it explains why purely biomedical interventions (surgery, injections, manual therapy) often fail in chronic pain β the neuroplastic changes must be addressed concurrently with tissue pathology.
Common Clinical Presentations:
- Frozen shoulder (adhesive capsulitis) β movement neglect drives progressive capsular fibrosis
- Complex Regional Pain Syndrome (CRPS) β severe movement neglect with autonomic changes
- Chronic low back pain β fear of spinal movement creates protective guarding
- Post-surgical pain syndromes β fear of re-injury perpetuates disability
- Chronic neck pain with reduced rotation
- Post-fracture stiffness beyond expected healing time
Metamodel Connections:
- Metamodel 0 (Evolutionary Mismatch): Modern sedentary lifestyle + safety culture amplifies protective responses; ancestral environments required movement despite minor injury
- Metamodel 1 (Selfish Systems): The Selfish Brain prioritizes threat avoidance over movement; selfish immune system may maintain low-grade inflammation to justify protective behavior
- Metamodel 2 (Stress Axes): Chronic HPS-axis activation from pain-related stress reinforces fear memories; cortisol dysregulation affects brain plasticity
- Metamodel 3 (Barriers): Movement neglect can be viewed as a neurological barrier β the brain creates a barrier to movement even when peripheral tissues are healed
Diagnostic Recognition:
- Laterality recognition test: Patient sees images of left/right hands/shoulders and identifies which side β neglected limb shows 200-500ms delay and reduced accuracy (<80%)
- Two-point discrimination: Compare affected to unaffected side β >5mm difference suggests sensory cortical reorganization
- Pain with imagined movement (motor imagery without actual movement)
- Disproportionate disability relative to tissue pathology on imaging
- "I can't move it" despite preserved strength on formal testing
Assessment Thresholds:
- Motor cortex representation reduction: 30-50% shrinkage measurable via TMS mapping (research setting)
- Two-point discrimination: Normal finger = 2-3mm, affected in neglect = 20-50mm increase
- Laterality recognition: >200ms slower than unaffected side; <80% accuracy
- Range of motion: Often <50% of expected despite healed tissues
Evidence-Based Intervention Protocol (Graded Motor Imagery - GMI):
Stage 1: Laterality Recognition Training (2-4 weeks)
- Patient views images of affected body part in various positions
- Task: quickly identify left vs right without moving
- Reactivates motor cortex representation without threat of actual movement
- 10-15 minutes, 3x daily; aim for >90% accuracy, <2s response time
Stage 2: Imagined Movement (2-4 weeks)
- Patient mentally rehearses previously painful movements
- Activates motor cortex without peripheral nociceptive input
- Use multisensory cues (visualize, feel, hear the movement)
- Start with non-painful movements, gradually approach feared movements
Stage 3: Mirror Therapy (2-4 weeks)
- Patient moves unaffected limb while viewing mirror reflection
- Brain perceives neglected limb moving normally without pain
- Reactivates motor cortex representation, reduces threat value
- 5-10 minutes, 2-3x daily; gradually increase movement complexity
Stage 4: Graded Actual Movement (ongoing)
- Very gradual, sub-threshold exposure to actual movement
- Combine with pain neuroscience education to reduce threat interpretation
- Use interoceptive awareness training to distinguish protective tension from tissue damage
- May combine with manual therapy to address secondary tissue restrictions
Concurrent Interventions:
- Pain Neuroscience Education: Explain brain plasticity, safety of movement, difference between hurt and harm
- Stress reduction: Address HPS axis dysfunction via breathwork, meditation, sleep optimization
- Anti-inflammatory nutrition: Reduce metaflammation that may sensitize nociceptors β omega-3s, SPMs, reduce refined carbohydrates
- Mirror neurons activation: Watching others perform the feared movement painlessly
- Exposure therapy: Graduated hierarchy of feared movements (behavioral psychology approach)
Why Standard PT Fails:
Forcing movement without addressing cortical reorganization and threat value increases distress, reinforces protective responses, and may worsen neglect. "No pain, no gain" directly contradicts neuroscience of movement neglect.
Prognosis:
- GMI protocol shows 50-70% reduction in pain and disability in studies
- Earlier intervention (within 6 months of pain onset) shows better outcomes
- Chronic neglect (>2 years) requires longer treatment (6+ months)
- Must address psychological factors concurrently (catastrophizing, fear-avoidance beliefs)
Cross-System Integration:
Movement neglect demonstrates immune-neuro-metabolic integration: initial inflammatory pain β neuroplastic changes β metabolic tissue degradation β re-injury risk β immune activation. Breaking this cycle requires addressing all three systems simultaneously.
ΒΆ Key Facts
- Motor cortex representation of neglected limb shrinks by 30-50% in chronic pain patients (measurable via transcranial magnetic stimulation mapping)
- Two-point discrimination threshold increases by 20-50mm in neglected body regions compared to unaffected side
- Laterality recognition (identifying left vs right images) slows by 200-500ms for neglected limbs; accuracy drops below 80%
- Mirror therapy creates visual illusion of normal pain-free movement, reactivating motor cortex without threatening actual movement
- Graded motor imagery sequence (laterality β imagined movement β mirror therapy β actual movement) shows 50-70% improvement in pain/disability
- Movement neglect shares brain activation patterns with phantom limb pain β both involve cortical reorganization and learned pain
- Early mobilization after injury (within pain tolerance, first 48-72 hours) prevents development of cortical neglect
- Movement neglect can occur without conscious awareness β patients often deny avoiding movement but demonstrate it behaviorally
- CRPS Type 1 shows most severe movement neglect with additional autonomic dysfunction (temperature/color changes)
- Forced movement without addressing fear-avoidance increases amygdala activation and can worsen neglect (iatrogenic harm)
- Brain imaging shows reduced BOLD signal in motor cortex when patients imagine moving neglected limb (reduced cortical engagement)
- GMI protocol requires minimum 2 weeks per stage (total 8-12 weeks) β faster progression reduces efficacy
- Movement neglect can spread to adjacent body parts (e.g., shoulder neglect extending to hand/fingers)
- Virtual reality showing normal movement can enhance mirror therapy effects (multisensory integration)
- Pain neuroscience education alone reduces movement neglect in 30-40% of patients (reduces threat value)
ΒΆ Connections
- Frozen shoulder β movement neglect is a primary mechanism driving progressive capsulitis and adhesion formation
- CRPS β complex regional pain syndrome represents most severe form of movement neglect with added sympathetic dysfunction
- fear-avoidance β fear of movement/re-injury is the psychological driver initiating neglect cascade
- cortical reorganization β the neuroplastic mechanism underlying motor and sensory map changes in neglect
- motor cortex β M1 representation of neglected body part undergoes maladaptive shrinkage and smudging
- mirror therapy β evidence-based treatment exploiting mirror neurons to reactivate motor cortex for neglected limb
- graded motor imagery β systematic GMI protocol (lateralityβimageryβmirrorβmovement) reverses cortical changes
- learned pain β expectation-based pain matrix activation perpetuates movement avoidance even without nociceptive input
- central sensitization β overlapping mechanism where pain becomes uncoupled from peripheral tissue state
- Amygdala β encodes threat memory associating movement with danger; drives fear-avoidance behavior
- anterior cingulate cortex β processes pain unpleasantness and generates emotional suffering from movement-related pain
- BDNF β brain-derived neurotrophic factor expression reduced in motor cortex with disuse; needed for neuroplastic recovery
- chronic pain syndromes β movement neglect is common mechanism across diverse chronic pain presentations
- neuroplasticity β both maladaptive (neglect development) and adaptive (recovery via GMI) plasticity are involved
- pain matrix β network of brain regions (insula, ACC, S1, prefrontal cortex) activated by movement intention in neglect
- periaqueductal gray (PAG) β fails to activate descending pain inhibition in movement neglect; instead facilitates pain
- basal ganglia β encodes habitual protective muscle guarding and compensatory movement patterns
- Cerebellum β adapts to altered movement strategies, reinforcing maladaptive motor programs
- proprioception β reduced proprioceptive input from disuse contributes to sensory cortical smudging
- NMDA receptor β upregulated in dorsal horn during central sensitization component of movement neglect
- inflammation β initial inflammatory pain triggers neglect; chronic low-grade inflammation may maintain it
- muscle atrophy β secondary consequence of movement neglect; disuse leads to protein breakdown exceeding synthesis
- Thoracolumbar Fascia (TLF) Innervation β fascial mechanoreceptor dysfunction develops with immobility in neglect
- pain neuroscience education β educational intervention reducing threat value of pain; effective adjunct to GMI
- interoception β training interoceptive awareness helps distinguish protective tension from actual tissue damage
- Cognitive Behavioral Therapy β addresses catastrophizing and fear-avoidance beliefs perpetuating neglect
- HPS-axis β chronic stress axis activation from pain reinforces threat memories; cortisol affects neuroplasticity
- Selfish Brain β brain prioritizes threat avoidance over movement function in neglect
- catastrophizing β pain catastrophizing thoughts amplify threat value and worsen movement neglect
- Body schema β outdated body representation in posterior parietal cortex contributes to motor planning deficits
ΒΆ Module References
- Module 1
ΒΆ From neuroscience/
ΒΆ Definition
Movement neglect is the reduced initiation, amplitude, or frequency of voluntary movement on one side of the body despite preserved motor strength and intact peripheral motor systems. Distinguished from paralysis (structural inability to generate movement) and apraxia (loss of motor planning capacity), movement neglect represents a failure of motor intention and drive. In cPNI, the term extends to protective immobilization behaviours in chronic pain syndromes where the motor cortex "forgets" how to use a body region despite tissue healing.
ΒΆ Picture It
Imagine a city where one entire district has been removed from the mayor's map. The roads still work, the buildings stand intact, the power lines carry electricityβbut City Hall has stopped sending maintenance crews, garbage collection, or repair teams to that neighbourhood. It's not that the infrastructure is broken; it's that the central command has de-prioritized that district so thoroughly that it might as well not exist. Eventually, the roads crack from disuse, weeds grow through pavement, and residents stop trying to report problems because no one responds. This is movement neglect: the brain's motor planning centres have erased a limb from their priority maps. The muscles can still contract (the roads still function), but the executive command to use them has been withdrawn. In chronic pain, this happens graduallyβeach painful movement is like a complaint call that gets ignored, until the brain simply stops sending commands to that body part altogether.
ΒΆ Mechanism
Movement neglect arises through distinct pathways depending on acute neurological injury versus chronic pain-driven mechanisms:
Classical neurological movement neglect:
- Right hemisphere parietal cortex damage (especially inferior parietal lobule) β disrupted spatial attention maps β reduced awareness of contralateral space
- Supplementary motor area (SMA) lesions β impaired motor intention generation β decreased voluntary movement initiation
- Premotor cortex damage β loss of motor preparation signals β reduced movement amplitude
- Basal ganglia dysfunction (particularly caudate/putamen) β dopaminergic pathway disruption β hypokinesia and bradykinesia
- Right hemisphere dominance: 70-85% of movement neglect occurs with right-sided lesions affecting left-sided movement due to right hemisphere's bilateral attentional capacity
Chronic pain-induced movement neglect cascade:
Molecular mechanisms in chronic pain neglect:
-
Inflammatory cytokine effects:
- IL-1Ξ² (>5 pg/mL CSF) β crosses blood-brain barrier β activates microglial IL-1R1 β NF-ΞΊB activation β reduced glutamate release in motor cortex
- TNF-Ξ± β TNFR1 signaling β decreased BDNF production β impaired motor cortex plasticity
- IL-6 (>10 pg/mL serum) β gp130 receptor activation β JAK-STAT3 pathway β altered motor neuron excitability
-
Cortical reorganization:
- Reduced use β decreased BDNF signaling β synaptic pruning in M1 motor cortex
- Shrinkage of cortical motor map territory by 30-50% (measurable via TMS motor mapping)
- Expansion of adjacent body part representations (e.g., hand area expands when shoulder becomes neglected)
- Decreased intracortical inhibition β paradoxical hyperexcitability with reduced voluntary output
-
Fear-avoidance circuitry:
- Pain experience β amygdala activation β CRH release β HPA axis activation
- Elevated cortisol β glucocorticoid receptor activation in prefrontal cortex β impaired top-down motor control
- Anterior cingulate cortex hyperactivity β enhanced pain anticipation β movement avoidance before pain onset
- Periaqueductal gray (PAG) activation β descending pain facilitation β amplified movement-related pain
-
Neuroplastic maladaptation:
- Repeated pain-movement pairing β long-term potentiation in pain pathways
- Mirror neuron system dysfunction β impaired motor imagery capacity
- Reduced proprioceptive feedback β distorted body schema representation
- Decreased Ξ³-aminobutyric acid (GABA) in motor cortex β loss of movement refinement
ΒΆ Clinical Significance
Movement neglect is a critical diagnostic indicator that pain pathology has transitioned from peripheral tissue damage to central nervous system reorganizationβthis marks the shift from acute to chronic pain in the cPNI framework.
Conditions where movement neglect is primary:
- Frozen shoulder: 85-90% demonstrate movement neglect behaviours independent of capsular restriction; patients often cannot initiate abduction even when passive range is greater
- Complex regional pain syndrome: Profound movement neglect with cortical reorganization measurable within 3-6 months; motor imagery breakdown precedes physical disability
- Chronic low back pain: Truncal movement restriction persists long after disc healing; 60% show fear-avoidance beliefs as primary driver
- Post-stroke upper limb: 30-40% develop learned non-use despite adequate motor capacity for functional tasks
Metamodel connections:
- Selfish brain: The brain withdraws motor resources from painful regions to conserve energy for threat monitoring and immune responses; movement neglect reflects the brain prioritizing safety over function
- Evolutionary mismatch: Acute pain evolved to enforce rest during healing; chronic activation of this protective mechanism in absence of tissue damage represents evolutionary overshoot
- Fear-avoidance model: Movement neglect is the behavioral endpoint of the fear β avoidance β disability cycle
Clinical thresholds and biomarkers:
- Motor cortex territory reduction >30% (TMS mapping) correlates with poor rehabilitation outcomes
- Fear-avoidance beliefs questionnaire (FABQ) scores >50 predict movement neglect development
- Pain catastrophizing scale (PCS) >30 strongly associates with learned non-use
- Serum IL-6 >10 pg/mL indicates systemic inflammation potentially affecting motor planning
- Motor imagery capacity <60% accuracy (left/right limb recognition tasks) indicates cortical reorganization
Intervention implications:
-
Graded motor imagery sequence (Moseley protocol):
- Phase 1: Left/right limb discrimination (pure cognitive, no movement) β restores motor cortex body maps
- Phase 2: Imagined movement (motor imagery) β activates motor planning without pain
- Phase 3: Mirror therapy β visual-motor incongruence retrains cortex
- Phase 4: Graded actual movement β graduated exposure breaks fear-avoidance
-
Address inflammatory drivers:
- Anti-inflammatory nutrition (Omega-3 >2g EPA+DHA daily, reduce Omega-6 to omega-3 ratio to
:1) - Specialized pro-resolving mediators supplementation to enhance inflammation resolution
- Target Gut permeability and Chronic low-grade inflammation
- Anti-inflammatory nutrition (Omega-3 >2g EPA+DHA daily, reduce Omega-6 to omega-3 ratio to
-
Pain neuroscience education:
- Explain cortical reorganization to reduce threat perception
- Demonstrate that pain β tissue damage in chronic states
- Reframe movement as safe and therapeutic rather than harmful
-
Neuroscience-informed physical therapy:
- Begin with non-painful movement to restore cortical maps before stretching into pain
- Use bilateral movement patterns to engage intact hemisphere
- Incorporate tactile discrimination training to restore sensory-motor integration
Critical clinical insight: Treating movement neglect with passive therapies (massage, manipulation, rest) reinforces the neglect. Active, graded, patient-controlled movement is essential to reverse cortical reorganization.
ΒΆ Key Facts
- 90% of frozen shoulder patients exhibit movement neglect behaviours that persist even after capsular inflammation resolves
- Cortical motor representation shrinks 30-50% in chronic regional pain syndromes, measurable via transcranial magnetic stimulation motor mapping
- Graded motor imagery protocols improve pain scores by 40-60% and function by 60-70% when combined with graduated movement exposure
- IL-1Ξ² administration (even 1 ng/kg) reduces voluntary movement initiation in animal models independent of tissue damageβdemonstrates direct cytokine effect on motor planning
- Mirror therapy activates bilateral premotor cortex and SMA without actual movement, allowing motor planning restoration before physical therapy
- Fear-avoidance beliefs (FABQ scores >50) predict disability more strongly than pain intensity, MRI findings, or physical examination results
- Movement neglect often persists 6-24 months after tissue healing, explaining the transition to chronic pain in 20-30% of acute injuries
- Left/right limb recognition accuracy drops to 50-60% (chance level) in chronic pain patients, indicating complete loss of motor cortex body maps
- Complex regional pain syndrome shows 25-35% reduction in motor cortex territory within 3 months of onset
- Anti-GAD65 antibodies in Stiff person syndrome create extreme movement neglect through GABAergic dysfunction, representing autoimmune movement restriction
- Motor imagery practice (15 minutes daily) can reverse cortical reorganization measurably within 4-6 weeks
- Movement neglect affects contralateral (opposite side) limbs in 15-20% of chronic pain cases due to bilateral cortical reorganization
ΒΆ Connections
- Frozen shoulder β archetypal movement neglect condition where capsular restriction is secondary to motor planning failure
- Chronic pain syndromes β movement neglect is the behavioral hallmark of centralized pain states
- Central sensitization β amplified pain processing drives fear-avoidance learning and movement suppression
- Fear-avoidance β psychological mechanism converting acute pain into chronic movement restriction
- Motor cortex β undergoes maladaptive reorganization with territory shrinkage in neglected body regions
- Neuroplasticity β bidirectional process underlying both development and resolution of movement neglect
- IL-1Ξ² β directly suppresses motor cortex activity and voluntary movement initiation independent of pain
- TNF-Ξ± β reduces BDNF production impairing motor learning and cortical map maintenance
- Inflammation β systemic inflammatory cytokines cross blood-brain barrier affecting motor planning regions
- Complex regional pain syndrome β severe movement neglect with profound cortical reorganization and dystonia
- Mirror therapy β intervention exploiting visual-motor systems to restore motor planning without movement
- Graded motor imagery β systematic rehabilitation progression from cognitive to actual movement
- Basal ganglia β striatal dopamine dysfunction contributes to hypokinesia in neurological movement neglect
- Premotor cortex β damage impairs motor intention generation and movement amplitude planning
- Pain neuroscience education β cognitive intervention reducing threat perception and fear-avoidance beliefs
- Learned non-use β behavioral conditioning where repeated pain-movement pairing extinguishes voluntary movement
- Physical therapy β must address cortical reorganization and fear-avoidance, not just peripheral tissue
- GAD65 β autoantibody target in stiff person syndrome causing GABAergic dysfunction and movement restriction
- Stiff person syndrome β autoimmune disorder featuring profound movement neglect through GABAergic system disruption
- Autoimmunity β anti-GAD65 antibodies demonstrate autoimmune mechanisms can directly cause movement disorders
- Rehabilitation β requires graduated exposure therapy to overcome learned movement suppression
- BDNF β critical neurotrophin for motor cortex plasticity; reduced levels impair motor learning
- Amygdala β fear conditioning center driving movement avoidance through threat detection
- Anterior cingulate cortex β hyperactivity in chronic pain creates anticipatory movement restriction
- HPA axis β chronic activation produces cortisol-mediated impairment of prefrontal motor control
- Proprioception β reduced feedback from immobilized regions distorts body schema and motor planning
- Chronic inflammation β sustained cytokine elevation affects brain motor systems creating sickness-like movement suppression
- Disability β movement neglect is stronger predictor of functional limitation than structural pathology
- Cortisol β chronically elevated levels impair prefrontal top-down control of movement initiation
ΒΆ Module References
- Module 1