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1.  The effects of preferential A- and C-fibre blocks and T-type calcium channel antagonist on detection of low-force monofilaments in healthy human participants 
BMC Neuroscience  2015;16:52.
A myriad of studies have argued that tactile sensibility is underpinned exclusively by large myelinated mechanoreceptors. However, the functional significance of their slow-conducting counterparts, termed C-low threshold mechanoreceptors (C-LTMRs), remains largely unexplored. We recently showed the emergence of brush- and vibration-evoked allodynia in human hairy and glabrous skin during background muscle pain. The allodynia persisted following the preferential blockade of myelinated fibres but was abolished by the preferential blockade of cutaneous C fibres, thereby suggesting a pathway involving hairy skin C-LTMRs and their functional counterparts in glabrous skin in this phenomenon. In the present study, we tested the effects of preferential A- and C-fibre conduction blocks and pharmacological blockade of T-type calcium channel Cav3.2 (expressed selectively on small-fibre LTMRs) on monofilament detection thresholds in healthy participants by compression, low-dose intradermal anaesthesia (xylocaine 0.25 %) and selective T-channel antagonist, TTA-A2.
We found that all participants could detect monofilament contacts (as low as 1.6 mN) within the innocuous tactile range regardless of the preferential blockade of myelinated fibres. Furthermore, during the compression block no subject reported a switch in modality from touch to pain. That is, the low-force monofilament contacts were always perceived as non-painful. However, there was a small but significant elevation of monofilament thresholds (~2 mN) in the glabrous skin following the compression block. Importantly, no differences were found in the thresholds across hairy and glabrous regions while the myelinated fibres were conducting or not. The preferential blockade of C fibres in the glabrous skin (with myelinated fibres intact) also resulted in a small but significant elevation of tactile thresholds. Furthermore, the use of T-channel blocker in the glabrous skin during compression block of myelinated fibres resulted in complete abolition of monofilament sensibility within the innocuous tactile range (tested up to ~20 mN).
These observations suggest that C-LTMRs need not be regarded as a redundant tactile system, but appear to complement normal large-myelinated-fibre tactile function. Convergent findings in glabrous and hairy skin lend support for an underlying system of innocuous mechanoreception with Cav3.2-expressing unmyelinated fibres.
PMCID: PMC4535530  PMID: 26268809
C-tactile fibre; Glabrous skin; Tactile detection; Calcium channel Cav3.2; von Frey filament
2.  Somatotopic mismatch following stroke: a pathophysiological condition escaping detection 
BMJ Case Reports  2012;2012:bcr2012006304.
Clinical evaluation of somatosensory deficits in stroke patients is very limited and usually does not include testing of somatotopic organisation, which is a prerequisite for meaningful interpretation of sensory input and sensorimotor control. Detailed tactile testing of the left hand of a 54-year-old patient suffering from sensory deficit and central pain after a right-sided stroke revealed severe distortion of somatotopic sensory maps as evidenced by incorrect localisation of the point stimuli. Unlike previously reported gross somatotopic remapping taking place within reduced representational space after lesion, this is the first case report revealing chaotic scrambled somatosensory maps. While the incidence of such scrambled somatotopic representation of tactile input is not yet known in stroke patients, current observations indicate that in-depth investigations of somatotopic organisation of affected area may reveal the underlying cause for various functional deficits including central pain. Thus, new rehabilitation strategies may need to be developed specifically for such patients.
PMCID: PMC4543302  PMID: 23045439
3.  Tactile Motion Adaptation Reduces Perceived Speed but Shows No Evidence of Direction Sensitivity 
PLoS ONE  2012;7(9):e45438.
While the directionality of tactile motion processing has been studied extensively, tactile speed processing and its relationship to direction is little-researched and poorly understood. We investigated this relationship in humans using the ‘tactile speed aftereffect’ (tSAE), in which the speed of motion appears slower following prolonged exposure to a moving surface.
We used psychophysical methods to test whether the tSAE is direction sensitive. After adapting to a ridged moving surface with one hand, participants compared the speed of test stimuli on the adapted and unadapted hands. We varied the direction of the adapting stimulus relative to the test stimulus.
Perceived speed of the surface moving at 81 mms−1 was reduced by about 30% regardless of the direction of the adapting stimulus (when adapted in the same direction, Mean reduction = 23 mms−1, SD = 11; with opposite direction, Mean reduction = 26 mms−1, SD = 9). In addition to a large reduction in perceived speed due to adaptation, we also report that this effect is not direction sensitive.
Tactile motion is susceptible to speed adaptation. This result complements previous reports of reliable direction aftereffects when using a dynamic test stimulus as together they describe how perception of a moving stimulus in touch depends on the immediate history of stimulation. Given that the tSAE is not direction sensitive, we argue that peripheral adaptation does not explain it, because primary afferents are direction sensitive with friction-creating stimuli like ours (thus motion in their preferred direction should result in greater adaptation, and if perceived speed were critically dependent on these afferents’ response intensity, the tSAE should be direction sensitive). The adaptation that reduces perceived speed therefore seems to be of central origin.
PMCID: PMC3454433  PMID: 23029010
4.  Modulation of Human Muscle Spindle Discharge by Arterial Pulsations - Functional Effects and Consequences 
PLoS ONE  2012;7(4):e35091.
Arterial pulsations are known to modulate muscle spindle firing; however, the physiological significance of such synchronised modulation has not been investigated. Unitary recordings were made from 75 human muscle spindle afferents innervating the pretibial muscles. The modulation of muscle spindle discharge by arterial pulsations was evaluated by R-wave triggered averaging and power spectral analysis. We describe various effects arterial pulsations may have on muscle spindle afferent discharge. Afferents could be “driven” by arterial pulsations, e.g., showing no other spontaneous activity than spikes generated with cardiac rhythmicity. Among afferents showing ongoing discharge that was not primarily related to cardiac rhythmicity we illustrate several mechanisms by which individual spikes may become phase-locked. However, in the majority of afferents the discharge rate was modulated by the pulse wave without spikes being phase locked. Then we assessed whether these influences changed in two physiological conditions in which a sustained increase in muscle sympathetic nerve activity was observed without activation of fusimotor neurones: a maximal inspiratory breath-hold, which causes a fall in systolic pressure, and acute muscle pain, which causes an increase in systolic pressure. The majority of primary muscle spindle afferents displayed pulse-wave modulation, but neither apnoea nor pain had any significant effect on the strength of this modulation, suggesting that the physiological noise injected by the arterial pulsations is robust and relatively insensitive to fluctuations in blood pressure. Within the afferent population there was a similar number of muscle spindles that were inhibited and that were excited by the arterial pulse wave, indicating that after signal integration at the population level, arterial pulsations of opposite polarity would cancel each other out. We speculate that with close-to-threshold stimuli the arterial pulsations may serve as an endogenous noise source that may synchronise the sporadic discharge within the afferent population and thus facilitate the detection of weak stimuli.
PMCID: PMC3328488  PMID: 22529975

Results 1-4 (4)