Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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We studied whether stimulation of the primary motor cortex (M1) attenuates pain-related spinal withdrawal responses of neuropathic and healthy control rats, and whether the descending antinociceptive effect is relayed through the noradrenergic locus coeruleus (LC). The assessments of the noxious heat-evoked limb withdrawals reflecting spinal nociception and recordings of single LC units were performed in spinal nerve-ligated neuropathic and sham-operated control rats under light pentobarbital anesthesia. Electric stimulation of M1 produced equally strong spinal antinociception in neuropathic and control rats. ⋯ Lidocaine block of the LC or block of descending noradrenergic influence by intrathecal administration of a alpha(2)-adrenoceptor antagonist failed to produce a significant attenuation of the spinal antinociceptive effect induced by electric M1 stimulation in the neuropathic or the sham group. The results indicate that stimulation of the rat M1 induces spinal antinociception in neuropathic as well as control conditions. While M1 stimulation may activate the LC, particularly in the neuropathic group, the contribution of coeruleospinal noradrenergic pathways may not be critical for the spinal antinociceptive effect induced by M1 stimulation.
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Previous studies have shown that walking is not a purely automatic motor task but places demands on sensory and cognitive systems. We set out to investigate whether complex walking tasks, as when walking down a steeper gradient while performing a concurrent cognitive task, would demand gait adaptation beyond those required for walking under low-challenge conditions. Thirteen healthy young individuals walked at their self-selected speed on a treadmill at different inclinations (0, -5 and -10%). ⋯ Compared to walking alone, walking under dual-task condition resulted in increased step width (P < 0.001), and increased medio-lateral (M-L) CoM displacement (P = 0.039) regardless of inclination grade, while sagittal plane dynamics did not change. Findings suggest that gait adapts differently to cognitive and mechanical constraints; the cognitive system is more actively involved in controlling frontal than sagittal plane gait dynamics, while the reverse is true for the mechanical system. Finally, these findings suggest that gait adaptations maintain the ability to perform concurrent tasks while treadmill walking in healthy young adults.
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Manipulation of cortical excitability can be experimentally achieved by the application of transcranial random noise stimulation (tRNS). TRNS is a novel method of non-invasive electrical brain stimulation whereby a random electrical oscillation spectrum is applied over the cortex. A previous study recently reported that application of weak 10-min tRNS over primary motor cortex (M1) enhances corticospinal excitability both during and after stimulation in the healthy human brain. ⋯ Our results indicate that tRNS applied with different durations and/or in combination with a task might result in different outcomes. Application of tRNS to the human cortex allows an unnoticeable and thus painless, selective, non-invasive and reversible activity change within the cortex, its main advantage being the direction insensitivity of the stimulation. TRNS also provides a qualitatively new way of producing and interfering with brain plasticity, although, further research is required to optimise stimulation parameters and efficacy.
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The aim of the current study was to evaluate bilaterally warm/cold detection and heat/cold pain thresholds over the hand/wrist in patients with carpal tunnel syndrome (CTS). A total of 25 women with strictly unilateral CTS (mean 42 +/- 10 years), and 20 healthy matched women (mean 41 +/- 8 years) were recruited. Warm/cold detection and heat/cold pain thresholds were assessed bilaterally over the carpal tunnel and the thenar eminence in a blinded design. ⋯ Our findings revealed bilateral thermal hyperalgesia (lower heat pain and reduced cold pain thresholds) but not hypoesthesia (normal warm/cold detection thresholds) in patients with strictly unilateral CTS when compared to controls. We suggest that bilateral heat and cold hyperalgesia may reflect impairments in central nociceptive processing in patients with unilateral CTS. The bilateral thermal hyperalgesia associated with pain intensity and duration of pain history supports a role of generalized sensitization mechanisms in the initiation, maintenance and spread of pain in CTS.
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Transient receptor potential receptors (TRP) on primary afferent neurons respond to noxious and/or thermal stimuli. TRPV1 receptors can be activated by noxious heat, acid, capsaicin and resiniferatoxin, leading to burning pain or itch mediated by discharges in C polymodal and Adelta mechano-heat nociceptors and in central neurons, including spinothalamic tract (STT) cells. Central nociceptive transmission involves both non-NMDA and NMDA receptors, and inhibitory interneurons as well as projection neurons contribute to the neural interactions. ⋯ Central sensitization depends on activation of several protein kinases and other enzymes, such as nitric oxide synthase. This process is regulated by protein phosphatases. Central sensitization can be regarded as a spinal cord form of long-term potentiation.