Sensory Dysfunction Associated With Repetitive Strain Injuries of Tendinitis and Focal Hand Dystonia: A Comparative Study

Byl, Nancy N.; Wilson, Frank; Merzenich, Michael M.; Melnick, Marsha E; Scott, Patrick A.; Oakes, Alison; McKenzie, Alison

doi:10.2519/jospt.1996.23.4.234

Cited by 120 publications

(57 citation statements)

References 26 publications

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“…Volume % degenerated fibers in rabbit muscles tibialis anterior (TA) and extensor digitorum longus (EDL) after several days of continuous and intermittent stimulation (data from [80]). muscle and extensor muscles are relatively high (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) [8,127,149] and comparable with firing rates of previously mentioned animal studies. The finding in the study of Lexell et al [80] that especially muscles subjected to continuous stimulation are at risk for degeneration provides strong support for the ''Cinderella hypothesis''.…”

Section: Cinderella Hypothesissupporting

confidence: 84%

“…Results from animal studies indicate that, in addition to the peripheral effects on sensory quality, changes in the cerebral cortex as a response to sustained repetitive muscle activity can occur [17][18][19]. In monkeys that performed highly stereotypical and spatially constrained and highly repetitive movements with one hand, changes in the cerebral cortex suggest a reduction in the differentiation of sensory information from the hand and arm [19]. It is therefore possible that pain impairs proprioception, which will lead to less precise motor control and possibly as a compensatory reaction, to an increased effort mainly in the form of increased coactivation of muscles.…”

Section: Feedback Loops From Muscle Disorder To Muscle Activitymentioning

confidence: 99%

“…A recent reformulation of the hypothesis of Johanssen and Sojka focuses on this aspect, where it is assumed that the reduced proprioception requires increased effort to maintain task performance, which might lead to a vicious circle [61]. Results from animal studies indicate that, in addition to the peripheral effects on sensory quality, changes in the cerebral cortex as a response to sustained repetitive muscle activity can occur [17][18][19]. In monkeys that performed highly stereotypical and spatially constrained and highly repetitive movements with one hand, changes in the cerebral cortex suggest a reduction in the differentiation of sensory information from the hand and arm [19].…”

Section: Feedback Loops From Muscle Disorder To Muscle Activitymentioning

confidence: 99%

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Erratum to “Pathophysiology of upper extremity muscle disorders” [Journal of Electromyography and Kinesiology 16 (2006) 1–16]

Visser

Dieën

2006

Journal of Electromyography and Kinesiology

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A review of the literature on the pathophysiology of upper extremity muscle disorders (UEMDs) was performed. An overview is given of clinical findings and hypotheses on the pathogenesis of UEMDs. The literature indicates that disorders of muscle cells and limitations of the local circulation underlie UEMDs. However, these disorders identified do not necessarily lead to symptoms. The following mechanisms have been proposed in the literature: (1) selective recruitment and overloading of type I (Cinderella) motor units; (2) intra-cellular Ca 2+ accumulation; (3) impaired blood flow; (3b) reperfusion injury; (3.3c) blood vessel-nociceptor interaction; (4a) myofascial force transmission; (4b) intramuscular shear forces; (5) trigger points; (6) impaired heat shock response. The results of the review indicate that there are multiple possible mechanisms, but none of the hypotheses forms a complete explanation and is sufficiently supported by empirical data. Overall, the literature indicates that: (1) sustained muscle activity, especially of type I motor units, may be a primary cause of UEMDs; (2) in UEMDs skeletal muscle may show changes in morphology, blood flow, and muscle activity; (3) accumulation of Ca 2+ in the sarcoplasm may be the cause of muscle cell damage; (4) it seems plausible that suboptimal blood flow plays a role in pathogenesis of UEMDs; (5) since the presence of fiber disorders is not a sufficient condition for the development of UEMSDs additional mechanisms, such as sensitization, are assumed to play a role.

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Section: Cinderella Hypothesissupporting

confidence: 84%

Section: Feedback Loops From Muscle Disorder To Muscle Activitymentioning

confidence: 99%

Section: Feedback Loops From Muscle Disorder To Muscle Activitymentioning

confidence: 99%

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Erratum to “Pathophysiology of upper extremity muscle disorders” [Journal of Electromyography and Kinesiology 16 (2006) 1–16]

Visser

Dieën

2006

Journal of Electromyography and Kinesiology

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“…There is strong evidence that repetitive tasks alone can lead to degradation of the somatosensory cortex in monkeys, 25,26,28,111 rats, 91 and humans (Table 4). 22,24,27 In the primate model of repetitive grasping, electrophysiological mapping of the primar y somatosensory cortex (the region of the dorsal parietal cortex designated as area SI) reveals a dedifferentiation of the hand region with shifted or degraded digit-receptive fields.…”

Section: Evidence Of Cns Reorganization In Wmsdsmentioning

confidence: 99%

Work-Related Musculoskeletal Disorders of the Hand and Wrist: Epidemiology, Pathophysiology, and Sensorimotor Changes

Barr

Barbe²,

Clark³

2004

J Orthop Sports Phys Ther

210

114

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The purpose of this commentary is to present recent epidemiological findings regarding work-related musculoskeletal disorders (WMSDs) of the hand and wrist, and to summarize experimental evidence of underlying tissue pathophysiology and sensorimotor changes in WMSDs. Sixty-five percent of the 333 800 newly reported cases of occupational illness in 2001 were attributed to repeated trauma. WMSDs of the hand and wrist are associated with the longest absences from work and are, therefore, associated with greater lost productivity and wages than those of other anatomical regions. Selected epidemiological studies of hand/wrist WMSDs published since 1998 are reviewed and summarized. Results from selected animal studies concerning underlying tissue pathophysiology in response to repetitive movement or tissue loading are reviewed and summarized. To the extent possible, corroborating evidence in human studies for various tissue pathomechanisms suggested in animal models is presented. Repetitive, handintensive movements, alone or in combination with other physical, nonphysical, and nonoccupational risk factors, contribute to the development of hand/wrist WMSDs. Possible pathophysiological mechanisms of tissue injury include inflammation followed by repair and/or fibrotic scarring, peripheral nerve injury, and central nervous system reorganization. Clinicians should consider all of these pathomechanisms when examining and treating patients with hand/wrist WMSDs.

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“…Focal hand dystonia is a motor disorder involving abnormal hand and finger positions, cramps, and noncoordinated movements of the hand and fingers (1)(2)(3)(4)(5)(6)(7)(8). It can be so disabling that patients have to limit or give up their occupation.…”

mentioning

confidence: 99%

Effective behavioral treatment of focal hand dystonia in musicians alters somatosensory cortical organization

Candia

Wienbruch

Elbert

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

158

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New perspectives in neurorehabilitation suggest that behavioral treatments of movement disorders may modify the functional organization of central somatosensory neural networks. On the basis of the assumption that use-dependent reorganization in these networks contributes to the fundamental abnormalities seen in focal dystonia, we treated 10 affected musicians and measured the concomitant somatosensory changes by using whole-head magnetoencephalography. We found that effective treatment, using the method of sensory motor retuning, leads to alterations in the functional organization of the somatosensory cortex. Specifically, before treatment, somatosensory relationships of the individual fingers differ between the affected and unaffected hands, whereas after treatment, finger representations contralateral to the dystonic side become more similar to the less-affected side. Further, somatosensory finger representations are ordered more according to homuncular principles after treatment. In addition, the observed physiologic changes correlated with behavioral data. These results confirm that plastic changes in parallel with emergent neurological dysfunction may be reversed by contextspecific, intensive training-based remediation.

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Sensory Dysfunction Associated With Repetitive Strain Injuries of Tendinitis and Focal Hand Dystonia: A Comparative Study

Cited by 120 publications

References 26 publications

Erratum to “Pathophysiology of upper extremity muscle disorders” [Journal of Electromyography and Kinesiology 16 (2006) 1–16]

Erratum to “Pathophysiology of upper extremity muscle disorders” [Journal of Electromyography and Kinesiology 16 (2006) 1–16]

Work-Related Musculoskeletal Disorders of the Hand and Wrist: Epidemiology, Pathophysiology, and Sensorimotor Changes

Effective behavioral treatment of focal hand dystonia in musicians alters somatosensory cortical organization

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