Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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Evidence by functional imaging studies suggests the role of left DLPFC in the inhibitory control of nociceptive transmission system. Pain exerts an inhibitory modulation on motor cortex, reducing MEP amplitude, while the effect of pain on motor intracortical excitability has not been studied so far. In the present study, we explored in healthy subjects the effect of capsaicin-induced pain and the modulatory influences of left DLPFC stimulation on motor corticospinal and intracortical excitability. ⋯ Capsaicin-induced pain significantly reduced test MEP amplitude and decreased SICI leaving ICF unchanged. Left DLPFC rTMS, together with the analgesic effect, was able to revert the effects of capsaicin-induced pain on motor cortex restoring normal MEP and SICI levels. These data support the notion that that tonic pain exerts modulatory influence on motor intracortical excitability; the activation of left DLPFC by hf rTMS could have analgesic effects, reverting also the motor cortex excitability changes induced by pain stimulation.
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Randomized Controlled Trial
Discharge of biceps brachii motor units is modulated by load compliance and forearm posture.
The purpose of this study was to compare the discharge characteristics of motor units in the biceps brachii during brief isometric contractions of the elbow flexors as subjects matched either a target force or a target joint angle with the forearm placed in one of two postures. One task required force control to exert a constant force against a rigid restraint (force task), whereas the other task involved position control to maintain a constant elbow angle while supporting an inertial load (position task). The left arm of right-handed subjects was rotated forward so that the upper arm was horizontal and the forearm was vertical. ⋯ Discharge rate was similar at the start of the force and position tasks in both the neutral posture (13.1 +/- 0.6 and 12.6 +/- 0.6 pps, P = 0.54) and the supinated posture (14.7 +/- 1.6 and 14.0 +/- 0.9 pps, P = 0.4) and declined during both tasks in the two forearm postures (P < 0.001). Nonetheless, the decrease in discharge rate (P < 0.001), increase in the coefficient of variation for interspike interval (P = 0.04), and increases in the standard deviation of acceleration (P = 0.02) were greatest for the position task in the supinated posture. These findings indicate that the influence of load compliance on the adjustments in motor unit activity during brief isometric contractions with the elbow flexors was modulated by changes in forearm posture.
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Memory problems are one of the most common symptoms of sport-related mild traumatic brain injury (MTBI), known as concussion. Surprisingly, little research has examined spatial memory in concussed athletes given its importance in athletic environments. Here, we combine functional magnetic resonance imaging (fMRI) with a virtual reality (VR) paradigm designed to investigate the possibility of residual functional deficits in recently concussed but asymptomatic individuals. ⋯ In addition, there was a significantly larger BOLD signal percent change at the right hippocampus. Neither cluster size nor BOLD signal percent change at shared ROIs was different between groups during retrieval. These major findings are discussed with respect to current hypotheses regarding the neural mechanism responsible for alteration of brain functions in a clinical setting.
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Our aim was to assess thermal sensitivity in both trigeminal and extra-trigeminal regions in patients with myofascial temporomandibular disorder (TMD) but without comorbid conditions as compared to age-matched controls. Twenty women (age 24 +/- 3 years) diagnosed with myofascial TMD according to the research diagnostic criteria for TMD and 20 healthy women (age 24 +/- 4 years) were included. Warm and cold detection thresholds (WDT and CDT, respectively) and heat and cold pain thresholds (HPT and CPT, respectively) were bilaterally assessed over the masseter and frontalis muscles (trigeminal regions) and the wrist (extra-trigeminal region). ⋯ CPT (P < 0.001) over the trigeminal area was positively correlated with both pain intensity and duration of pain symptoms: the longer the history of pain or the greater the pain intensity, the higher the CPT (i.e., the greater cold hyperalgesia) over the trigeminal region. Our findings revealed bilateral thermal hyperalgesia (lower HPT and higher CPT) but normal WDT and CDT in trigeminal and extra-trigeminal regions in women with myofascial TMD as compared to healthy controls. Bilateral heat/cold hyperalgesia in trigeminal and extra-trigeminal areas may reflect a dysfunction of thermal channels in myofascial TMD patients as result of some combination of peripheral sensitization, facilitation of central nociceptive processing and/or decreased descending inhibition.
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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.