Effects of fatigue induced by repetitive movements and isometric tasks on reaction time.

PURPOSE: The understanding of fatigue of the human motor system is important in the fields of ergonomics, sport, rehabilitation and neurology. In order to understand the interactions between fatigue and reaction time, we evaluated the effects of two different fatiguing tasks on reaction time. METHODS: 83 healthy subjects were included in a case-control study with three arms where single and double choice reaction time tasks were performed before and after 2 min fatiguing task (an isometric task, a finger tapping task and at rest). RESULTS: After an isometric task, the right-fatigued hand was slower in the choice component of a double choice reaction time task (calculated as the individual difference between single and double choice reaction times); also, the subjects that felt more fatigued had slower choice reaction time respect to the baseline assessment. Moreover, in relationship to the performance decay after two minutes, finger tapping task produces more intense fatigability perception. CONCLUSIONS: We confirmed that two minutes of isometric or repetitive tasks are enough to produce fatigue. The fatigue perception is more intense for finger tapping tasks in relation to the performance decay. We therefore confirmed that the two fatiguing tasks produced two different kind of fatigue demonstrating that with a very simple protocol it is possible to test subjects or patients to quantify different form of fatigue.

Effects of Moderate Static Magnetic Field on Neural Systems Is a Non-invasive Mechanical Stimulation of the Brain Possible Theoretically?

Static magnetic fields have been shown to induce effects on the human brain. Different experiments seem to support the idea that moderate static magnetic field can exert some influence on the gating processes of the membrane channels. In this article we visit the order of magnitude of the energy magnetic terms associated with moderate applied field (between 10 and 200 milliteslas). It is shown that gradients of the Zeeman energy associated with the inhomogeneous applied fields can induce pressures of the order of 10-2Pa. The surface tension generated by the magnetic pressure, on the surface delimiting the brain region subject to relevant field and gradients, is found to range between 10-1 and 1 mN⋅m-1. These pressures seem to be strong enough to interfere with the elastic and electrostatic energies involved in the channel activation-inactivation-deactivation mechanisms of biological membranes. It has been described that small mechanical force can activate voltage gated potassium channels. Moreover, stretch-activated ion channels are widely described in different biological tissues. Virtually, all these channels can modify their activity if stressed by a sufficient pressure delivered for enough time. We propose mechanical stimulation - possibly not exclusively - as a candidate mechanism how static magnetic field can produce effects in biological systems. It must be emphasized, that such field gradients were not previously proposed as a possible source of neural activity modification.

Development of chronic pain in males with traumatic spinal cord injury: role of circulating levels of the chemokines CCL2 and CXCL10 in subacute stage.

STUDY DESIGN: Longitudinal study. OBJECTIVES: To assess the impact of spinal cord injury (SCI) on circulating levels of chemokines (CCL2 and CXCL10) and its relation with pain development. SETTING: National Hospital for SCI patients. METHODS: We longitudinally studied changes in the circulating levels of CCL2 and CXCL10 in 27 male patients with complete SCI who were evaluated in the early subacute phase and indeed 3 and 6 months after injury measuring at each time-point serum levels of CCL2 and CXCL10. Patients were telephonically interviewed about pain 1 year after SCI. RESULTS: In the early subacute phase, patients with pain showed higher CXCL10 and similar CCL2 levels as opposed to those without pain. Moreover, CCL2 concentrations were positively associated with pain intensity. The results obtained by analysing the temporal profile of the chemokines suggested that CXCL10 was inclined to decrease over time, while CCL2 increased over time. CONCLUSION: The results of this preliminary study, the first performed in humans with traumatic SCI, suggest a link between changes in the circulating chemokine profile and pain development in subacute SCI stage as well as with severity in a more chronic stage. Large series studies will evaluate whether the circulating chemokine status can be useful as a biomarker for assessing the patients' risk for pain development.

Fatigue in Multiple Sclerosis: General and Perceived Fatigue Does Not Depend on Corticospinal Tract Dysfunction.

Background: Multiple sclerosis (MS) is an autoimmune disorder of the CNS in which inflammation, demyelination, and axonal damage of the central nervous system coexist. Fatigue is one of the most disabling symptoms in MS and little is known about the neurophysiological mechanisms involved. Methods: To give more mechanistic insight of fatigue in MS, we studied a cohort of 17 MS patients and a group of 16 age-matched healthy controls. Baseline Fatigue Severity Scales and Fatigue Rating were obtained from both groups to check the level of fatigue and to perform statistical correlations with fatigue-induced neurophysiologic changes. To induce fatigue we used a handgrip task. During the fatiguing task, we evaluated fatigue state (using a dynamometer) and after the task we evaluated the Borg Rating of Perceived Exertion Scale. Transcranial magnetic stimulation and peripheral electric stimulation were used to assess corticospinal tract and peripheral system functions before and after the task. Results: Clinically significant fatigue and central motor conduction time were greater in patients than in controls, while motor cortex excitability was decreased and maximal handgrip strength reduced in patients. Interestingly, fatigue state was positively correlated to perceived fatigue in controls but not in patients. Furthermore, in the presence of similar fatigue state over time, controls showed a significant fatigue-related reduction in motor evoked potential (a putative marker of central fatigue) whereas this effect was not seen in patients. Conclusions: in MS patients the pathogenesis of fatigue seems not driven by the mechanisms directly related to corticospinal function (that characterize fatigue in controls) but seems probably due to other "central abnormalities" upstream to primary motor cortex.