Brian D. Clark

Median nerve trauma in a rat model of work-related musculoskeletal disorder.

Anatomical and physiological changes were evaluated in the median nerves of rats trained to perform repetitive reaching. Motor degradation was evident after 4 weeks. ED1-immunoreactive macrophages were seen in the transcarpal region of the median nerve of both forelimbs by 5-6 weeks. Fibrosis, characterized by increased immunoexpression of collagen type I by 8 weeks and connective tissue growth factor by 12 weeks, was evident. The conduction velocity (NCV) within the carpal tunnel showed a modest but significant decline after 9-12 weeks. The lowest NCV values were found in animals that refused to participate in the task for the full time available. Thus, both anatomical and physiological signs of progressive tissue damage were present in this model. These results, together with other recent findings indicate that work-related carpal tunnel syndrome develops through mechanisms that include injury, inflammation, fibrosis and subsequent nerve compression.

Systemic inflammatory mediators contribute to widespread effects in work-related musculoskeletal disorders.

BARR, A.E., M.F. BARBE, and B.D. CLARK. Systemic inflammatory mediators contribute to widespread effects in work-related musculoskeletal disorders. Exerc. Sport Sci. Rev., Vol. 32, No. 4, pp. 135–142, 2004. Recent studies in a rat model have indicated that the pathophysiological mechanisms underlying development of work-related musculoskeletal disorders (WMSDs) include widespread inflammation and subsequent fibrosis at high levels of repetition and force. A systemic inflammatory component may affect tissues not directly involved in task performance, thereby contributing to widespread and puzzling symptoms that are often characteristic of patients with WMSDs.

Are there Important Exceptions to the Size Principle of α-Motoneurone Recruitment?

The size principle states that motoneurones are recruited in a sequence that follows a size rule; small motoneurones are recruited before large ones. By extension, exceptions to the principle would be identified when that size order is reversed for motoneurones within a functional group. At first glance, and ignoring for the moment the exact meaning of motoneurone size, these notions appear unambiguous. Some uncertainty arises, however, as to the nature of the experimental observations that would be necessary and sufficient to demonstrate exceptions to the size principle. In addition, it is unclear whether any such exceptions should be regarded as important to our understanding of neuromotor operation or function.

Frequency-dependent synaptic depression modifies postsynaptic firing probability in cats

1 The influence of stimulus trains applied to single I a axons on the firing behaviour of single motoneurones was assessed in anaesthetized cats. The change in motoneurone firing probability associated with a single I a afferent spike was measured from short‐latency peaks in peristimulus time histograms or cross‐correlograms. Some synapses showed frequency‐dependent depression of the short‐latency peak, which is consonant with the frequency‐dependent depression reported for the I a‐motoneurone excitatory postsynaptic potential (EPSP). 2 Where they could be measured, EPSPs superimposed on the depolarizing ramps of potential recorded from motoneurones as they fired repetitively showed frequency‐dependent changes in amplitude that parallelled those of the simultaneously recorded histograms. 3 Thus it appears that at synapses with small EPSPs, which are typical in the mammalian CNS, modulation of the EPSP should result in similar modulation of cell firing.