Muscle Hyperalgesia Correlates With Motor Function in Complex Regional Pain Syndrome Type 1.
van Rooijen DE, Marinus J, Schouten AC, Noldus LP, van Hilten JJ.
At present it is unclear if disturbed sensory processing plays a role in the development of the commonly observed motor impairments in patients with complex regional pain syndrome (CRPS). This study aims to investigate the relation between sensory and motor functioning in CRPS patients with and without dystonia. Patients with CRPS of the arm and controls underwent comprehensive quantitative sensory testing and kinematic analysis of repetitive finger movements. Both CRPS groups showed thermal hypoesthesia to cold and warm stimuli and hyperalgesia to cold stimuli. A decreased pressure pain threshold reflecting muscle hyperalgesia emerged as the most prominent sensory abnormality in both patient groups and was most pronounced in CRPS patients with dystonia. Moreover, the decreased pressure pain threshold was the only nociceptive parameter that related to measures of motor function in both patients and controls. CRPS patients with dystonia had an increased 2-point discrimination as compared to controls and CRPS patients without dystonia. This finding was also reported in other types of dystonia and has been associated to cortical reorganization in response to impaired motor function. We hypothesize that increased sensitivity of the circuitry mediating muscle nociception may play a crucial role in impaired motor control in CRPS. PERSPECTIVE: This is the first study linking a sensory dysfunction, ie, muscle hyperalgesia, to motor impairment in CRPS. Circuitries mediating muscle nociception may therefore play an important role in impaired motor control in CRPS.
Integration of Sensory Force Feedback Is Disturbed in CRPS-Related Dystonia.
Mugge W, van der Helm FC, Schouten AC.
Complex regional pain syndrome (CRPS) is characterized by pain and disturbed blood flow, temperature regulation and motor control. Approximately 25% of cases develop fixed dystonia. The origin of this movement disorder is poorly understood, although recent insights suggest involvement of disturbed force feedback. Assessment of sensorimotor integration may provide insight into the pathophysiology of fixed dystonia. Sensory weighting is the process of integrating and weighting sensory feedback channels in the central nervous system to improve the state estimate. It was hypothesized that patients with CRPS-related dystonia bias sensory weighting of force and position toward position due to the unreliability of force feedback. The current study provides experimental evidence for dysfunctional sensory integration in fixed dystonia, showing that CRPS-patients with fixed dystonia weight force and position feedback differently than controls do. The study shows reduced force feedback weights in CRPS-patients with fixed dystonia, making it the first to demonstrate disturbed integration of force feedback in fixed dystonia, an important step towards understanding the pathophysiology of fixed dystonia.
Fixed dystonia in complex regional pain syndrome: a descriptive and computational modeling approach.
Munts AG, Mugge W, Meurs TS, Schouten AC, Marinus J, Moseley GL, van der Helm FC, van Hilten JJ.
Complex regional pain syndrome (CRPS) may occur after trauma, usually to one limb, and is characterized by pain and disturbed blood flow, temperature regulation and motor control. Approximately 25% of cases develop fixed dystonia. Involvement of dysfunctional GABAergic interneurons has been suggested, however the mechanisms that underpin fixed dystonia are still unknown. We hypothesized that dystonia could be the result of aberrant proprioceptive reflex strengths of position, velocity or force feedback.
We systematically characterized the pattern of dystonia in 85 CRPS-patients with dystonia according to the posture held at each joint of the affected limb. We compared the patterns with a neuromuscular computer model simulating aberrations of proprioceptive reflexes. The computer model consists of an antagonistic muscle pair with explicit contributions of the musculotendinous system and reflex pathways originating from muscle spindles and Golgi tendon organs, with time delays reflective of neural latencies. Three scenarios were simulated with the model: (i) increased reflex sensitivity (increased sensitivity of the agonistic and antagonistic reflex loops); (ii) imbalanced reflex sensitivity (increased sensitivity of the agonistic reflex loop); (iii) imbalanced reflex offset (an offset to the reflex output of the agonistic proprioceptors).
For the arm, fixed postures were present in 123 arms of 77 patients. The dominant pattern involved flexion of the fingers (116/123), the wrists (41/123) and elbows (38/123). For the leg, fixed postures were present in 114 legs of 77 patients. The dominant pattern was plantar flexion of the toes (55/114 legs), plantar flexion and inversion of the ankle (73/114) and flexion of the knee (55/114).Only the computer simulations of imbalanced reflex sensitivity to muscle force from Golgi tendon organs caused patterns that closely resembled the observed patient characteristics. In parallel experiments using robot manipulators we have shown that patients with dystonia were less able to adapt their force feedback strength.
Findings derived from a neuromuscular model suggest that aberrant force feedback regulation from Golgi tendon organs involving an inhibitory interneuron may underpin the typical fixed flexion postures in CRPS patients with dystonia.
Modeling movement disorders–CRPS-related dystonia explained by abnormal proprioceptive reflexes.
Mugge W, Munts AG, Schouten AC, van der Helm FC.
Humans control their movements using adaptive proprioceptive feedback from muscle afferents. The interaction between proprioceptive reflexes and biomechanical properties of the limb is essential in understanding the etiology of movement disorders. A non-linear neuromuscular model of the wrist incorporating muscle dynamics and neural control was developed to test hypotheses on fixed dystonia. Dystonia entails sustained muscle contractions resulting in abnormal postures. Lack of inhibition is often hypothesized to result in hyperreflexia (exaggerated reflexes), which may cause fixed dystonia. In this study the model-simulated behavior in case of several abnormal reflex settings was compared to the clinical features of dystonia: abnormal posture, sustained muscle contraction, increased stiffness, diminished voluntary control and activity-aggravation. The simulation results were rated to criteria based on characteristic features of dystonia. Three abnormal reflex scenarios were tested: (1) increased reflex sensitivity-increased sensitivity of both the agonistic and antagonistic reflex pathways; (2) imbalanced reflex offset-a static offset to the reflex pathways on the agonistic side only; and (3) imbalanced reflex sensitivity-increased sensitivity of only the agonistic reflex pathways. Increased reflex sensitivity did not fully account for the features of dystonia, despite distinct motor dysfunction, since no abnormal postures occurred. Although imbalanced reflex offset did result in an abnormal posture, it could not satisfy other criteria. Nevertheless, imbalanced reflex sensitivity with unstable force feedback in one of the antagonists closely resembled all features of dystonia. The developed neuromuscular model is an effective tool to test hypotheses on the underlying pathophysiology of movement disorders.
In our CRPS clinic the patients who present have issues with movement. Some due to the pain or fear of pain and others with a fixed dystonia. Research demonstrates that there are changes in the motor and sensory areas of the brain that we can now target with clinic-based therapies.
CRPS Clinic – see here
Dystonia Clinic – see here