Search

Our understanding of how the mammalian somatosensory system detects noxious cold is still limited. While the role of TRPM8 in signaling mild non-noxious coolness is reasonably understood, the molecular identity of channels transducing painful cold stimuli remains unresolved. TRPC5 was originally described to contribute to moderate cold responses of dorsal root ganglia neurons in vitro, but mice lacking TRPC5 exhibited no change in behavioral responses to cold temperature. The question of why a channel endowed with the ability to be activated by cooling contributes to the cold response only under certain conditions is currently being intensively studied. It seems increasingly likely that the physiological detection of cold temperatures involves multiple different channels and mechanisms that modulate the threshold and intensity of perception. In this review, we aim to outline how TRPC5 may contribute to these mechanisms and what molecular features are important for its role as a cold sensor. [ABSTRACT FROM AUTHOR]

Medium-chain triglyceride (MCT) oil and fat are considered potential candidates to satisfy the nutritional demands of the increasing number of older patients requiring both dysphagia rehabilitation and nutritional therapy. Crystalline oil and fat (COF) is a unique material comprising MCT. In this study, we aimed to investigate the ways in which COF produces a cold sensation in the mouth, and assessed its facilitatory effect on swallowing initiation through two experiments. The first experiment, involving 27 participants, revealed that COF significantly reduced the onset latency of cold sensation and prolonged its duration compared to that of the control. The second experiment, involving 20 participants, revealed that the number of swallows significantly increased after swallowing COF. Our study confirms that the application of COF to the tongue induces a cold sensation and facilitates voluntary swallowing initiation. Therefore, COF holds great potential for aiding dysphagic patients.

Parkinson's disease (PD) is the second-most common neurodegenerative disorder worldwide and is diagnosed based on motor impairments. Non-motor symptoms are also well-recognised in this disorder, and peripheral neuropathy is a frequent but poorly appreciated non-motor sign. Studying how central and peripheral sensory systems are affected can contribute to the development of targeted therapies and deepen our understanding of the pathophysiology of PD. Although the cause of sporadic PD is unknown, chronic exposure to the pesticide rotenone in humans increases the risk of developing the disease. Here, we aimed to investigate whether peripheral neuropathy is present in a traditional model of PD. Mice receiving intrastriatal rotenone showed greatly reduced dopamine terminals in the striatum and a reduction in tyrosine hydroxylase-positive neurons in the Substantia nigra pars compacta and developed progressive motor impairments in hindlimb stepping and rotarod but no change in spontaneous activity. Interestingly, repeated testing using gold-standard protocols showed no change in gut motility, a well-known non-motor symptom of PD. Importantly, we did not observe any change in heat, cold, or touch sensitivity, again based upon repeated testing with well-validated protocols that were statistically well powered. Therefore, this traditional model fails to replicate PD, and our data again reiterate the importance of the periphery to the disorder. [ABSTRACT FROM AUTHOR]

Hesperetin, a citrus flavonoid, exerts vasodilation and is expected to improve endothelial function and alleviate cold sensation by activating nervous system thermal transduction pathways. In this randomized, double-blind, crossover, and placebo-controlled study, the purpose was to assess the effect of an orally administered highly bioavailable soluble inclusion complex of hesperetine-7-O-glucoside with β-cyclodextrin (HEPT7G/βCD; SunActive® HES/HCD) on cold sensation response during localized cold-stimulated stress in healthy humans. A significant (p ≤ 0.05) dose-dependent increase in skin cutaneous blood flow following relatively small doses of HEPT7G/βCD inclusion complex ingestion was confirmed, which led to a relatively effective recovery of peripheral skin temperature. The time delay of an increase in blood flow during rewarming varied significantly between low- and high-dose HEPT7G/βCD inclusion complex consumption (e.g., 150 mg and 300 mg contain 19.5 mg and 39 mg of HEPT7G, respectively). In conclusion, the substantial alteration in peripheral skin blood flow observed during local cooling stress compared to placebo suggested that deconjugated hesperetin metabolites may have a distinct capacity for thermoregulatory control of human skin blood flow to maintain a constant body temperature during cold stress exposure via cutaneous vasodilation and vasoconstriction systems. [ABSTRACT FROM AUTHOR]

Parkinson’s disease (PD) is the second-most common neurodegenerative disorder worldwide and is diagnosed based on motor impairments. Non-motor symptoms are also well-recognised in this disorder, and peripheral neuropathy is a frequent but poorly appreciated non-motor sign. Studying how central and peripheral sensory systems are affected can contribute to the development of targeted therapies and deepen our understanding of the pathophysiology of PD. Although the cause of sporadic PD is unknown, chronic exposure to the pesticide rotenone in humans increases the risk of developing the disease. Here, we aimed to investigate whether peripheral neuropathy is present in a traditional model of PD. Mice receiving intrastriatal rotenone showed greatly reduced dopamine terminals in the striatum and a reduction in tyrosine hydroxylase-positive neurons in the Substantia nigra pars compacta and developed progressive motor impairments in hindlimb stepping and rotarod but no change in spontaneous activity. Interestingly, repeated testing using gold-standard protocols showed no change in gut motility, a well-known non-motor symptom of PD. Importantly, we did not observe any change in heat, cold, or touch sensitivity, again based upon repeated testing with well-validated protocols that were statistically well powered. Therefore, this traditional model fails to replicate PD, and our data again reiterate the importance of the periphery to the disorder.

Copyright of Basic Sciences Journal of Textile Universities / Fangzhi Gaoxiao Jichu Kexue Xuebao is the property of Basic Sciences Journal of Textile Universities and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Moderate coolness is sensed by TRPM8 ion channels in peripheral sensory nerves, but the mechanism by which noxious cold is detected remains elusive. Here, we show that somatosensory and sympathetic neurons express two distinct mechanisms to detect noxious cold. In the first, inhibition by cold of a background outward current causes membrane depolarization that activates an inward current through voltage‐dependent calcium (CaV) channels. A second cold‐activated mechanism is independent of membrane voltage, is inhibited by blockers of ORAI ion channels and by downregulation of STIM1, and is recapitulated in HEK293 cells by co‐expression of ORAI1 and STIM1. Using total internal reflection fluorescence microscopy we found that cold causes STIM1 to aggregate with and activate ORAI1 ion channels, in a mechanism similar to that underlying store‐operated calcium entry (SOCE), but directly activated by cold and not by emptying of calcium stores. This novel mechanism may explain the phenomenon of cold‐induced vasodilation (CIVD), in which extreme cold increases blood flow in order to preserve the integrity of peripheral tissues. Synopsis: Extreme cold is not sensed via TRPM8 ion channels but by unclear alternative mechanisms. Here, we show that extreme cold causes STIM1‐mediated aggregation and activation of ORAI calcium channels in somatosensory and sympathetic neurons. Extreme cold (mean threshold 9–10°C) causes the ER‐resident membrane protein STIM1 to aggregate into puncta.STIM1 aggregation triggers aggregation of surface‐membrane calcium‐selective ORAI1 channels.The subsequent opening of ORAI1 channels causes a calcium influx without detectable membrane depolarization.Operation of this mechanism in sympathetic neurons may explain the phenomenon of cold‐induced vasodilation that increases blood flow in order to protect exposed tissues from frostbite. [ABSTRACT FROM AUTHOR]

[Display omitted] • Crystalline oil and fat (COF) exhibiting potential for dysphagic patient treatment. • COF reduced the onset latency of cold sensation and prolonged its duration. • The number of swallows significantly increased after swallowing COF. • COF application induces a cold sensation and facilitates swallowing initiation. Medium-chain triglyceride (MCT) oil and fat are considered potential candidates to satisfy the nutritional demands of the increasing number of older patients requiring both dysphagia rehabilitation and nutritional therapy. Crystalline oil and fat (COF) is a unique material comprising MCT. In this study, we aimed to investigate the ways in which COF produces a cold sensation in the mouth, and assessed its facilitatory effect on swallowing initiation through two experiments. The first experiment, involving 27 participants, revealed that COF significantly reduced the onset latency of cold sensation and prolonged its duration compared to that of the control. The second experiment, involving 20 participants, revealed that the number of swallows significantly increased after swallowing COF. Our study confirms that the application of COF to the tongue induces a cold sensation and facilitates voluntary swallowing initiation. Therefore, COF holds great potential for aiding dysphagic patients. [ABSTRACT FROM AUTHOR]

The purpose of this study was to clarify the effect of aerobic exercise training on the coldness of the body and physiologically-related factors in Japanese young women with cold constitution. Eighteen subjects were divided into two groups: exercise (E) and non-exercise control (C) groups. Subjects in the E group performed exercise training of fast walking 4 days or more per week for 4 weeks. The training significantly decreased the scores for cold feeling in the fingertips and toes, but did not change the metabolic rate or sublingual and skin temperatures in the hands and feet during rest under normothermic conditions. In the C group, all variables remained unchanged throughout the 4-week control period. These results suggest that aerobic exercise mitigated coldness in the distal portion of the extremities via the reduction of cold sensation at a normal body temperature in young women complaining of chilliness.

Hesperetin, a citrus flavonoid, exerts vasodilation and is expected to improve endothelial function and alleviate cold sensation by activating nervous system thermal transduction pathways. In this randomized, double-blind, crossover, and placebo-controlled study, the purpose was to assess the effect of an orally administered highly bioavailable soluble inclusion complex of hesperetine-7-O-glucoside with β-cyclodextrin (HEPT7G/βCD; SunActive® HES/HCD) on cold sensation response during localized cold-stimulated stress in healthy humans. A significant (p ≤ 0.05) dose-dependent increase in skin cutaneous blood flow following relatively small doses of HEPT7G/βCD inclusion complex ingestion was confirmed, which led to a relatively effective recovery of peripheral skin temperature. The time delay of an increase in blood flow during rewarming varied significantly between low- and high-dose HEPT7G/βCD inclusion complex consumption (e.g., 150 mg and 300 mg contain 19.5 mg and 39 mg of HEPT7G, respectively). In conclusion, the substantial alteration in peripheral skin blood flow observed during local cooling stress compared to placebo suggested that deconjugated hesperetin metabolites may have a distinct capacity for thermoregulatory control of human skin blood flow to maintain a constant body temperature during cold stress exposure via cutaneous vasodilation and vasoconstriction systems.

Cold sensations of varying intensities are perceived when human skin is subject to diverse environments. The accurate presentation of temperature changes is important to elicit immersive sensations in applications such as virtual reality. In this article, we developed a method to elicit intensity-adjustable non-contact cold sensations based on the vortex effect. We applied this effect to generate cold air at approximately 0 $^\circ$ C and varied the skin temperature over a wide range. The perception of different temperatures can be elicited by adjusting the volume flow rate of the cold air. Additionally, we introduced a cooling model to relate the changes in skin temperature to various parameters such as the cold air volume flow rate and distance from the cold air outlet to the skin. For validation, we conducted measurement experiments and found that our model can estimate the change in skin temperature with a root mean-square error of 0.16 $^\circ$ C. Furthermore, we evaluated the performance of a prototype in psychophysical cold discrimination experiments based on the discrimination threshold. Thus, cold sensations of varying intensities can be generated by varying the parameters. These cold sensations can be combined with images, sounds, and other stimuli to create an immersive and realistic artificial environment. [ABSTRACT FROM AUTHOR]

• Thermal stimuli with decreasing intensity from 40 °C elicit a cool sensation, with a detection threshold of 35 °C. • Thermal stimuli elicit evoked potentials with an N2P2 component whose latency is within the Aδ fiber range and amplitude is positively correlated with cooling amplitude. • Cold temperature discrimination starts to increase below 32 °C, peaks at 20 °C, and then decreases for temperatures below 16 °C. To evaluate the activity of cold Aδ-type fibers to thermal stimuli above human skin temperature (i.e., >32 °C). Twenty young adults aged 20–24 years participated in this study. The cold-detection threshold was measured from a basal temperature of 40 °C using an adaptive staircase method with high-speed cooling ramps (170 °C/s). A total of 150 stimulations at 36 °C, 32 °C, 28 °C, 24 °C, 20 °C, 16 °C, 12 °C, 8 °C, 4 °C and 0 °C (15 each) were performed. After each stimulation, subjects estimated the intensity of cold sensation using a visual analog scale, and evoked potentials were recorded. The average cold-detection threshold was 35 °C (SD = 1.8). Regardless of the stimulation temperature, subjects reported a cooling sensation. Interestingly, reported increments in sensation were prominent for stimulation temperatures between 32 °C and 20 °C, but below this latter temperature sensations varied only very slightly. Evoked potential recordings revealed that decreasing temperature stimuli from a baseline of 40 °C induced a previously unreported N2P2 component with a mean N2 peak latency of 275 ms (SD = 13.1). The peak-to-peak amplitude of the N2P2 complex increased as the intensity of the cooling stimulation increased, exhibiting a profile comparable to subject-perceived intensity, namely, a major increase up to 20 °C, followed by a plateau to 0 °C. The cool sensations reported by subjects were likely conveyed by Aδ fibers rather than by slow-conducting C fibers. Moreover, our rapid stimulation technique starting from a high temperature (40 °C) was capable of a) generating cold sensations at stimulation temperatures between 36 °C and 32 °C, and b) revealing the optimal activation range of Aδ fibers (20 °C–28 °C). Any decrease in temperature below this range did not result in a significant increase in sensation and thus probably did not evoke a significant increase in Aδ fiber activity. The regular assessment of cold sensation in peripheral neuropathies (i.e., with temperatures below 32 °C), could be completed by investigating cold-detection thresholds at temperatures ranging from 40 °C to 32 °C. Indeed, the absolute threshold of cold perception appears to start at 35 °C. Changes in the activation threshold of cold fibers were more easily detectable at this level. [ABSTRACT FROM AUTHOR]

Low temperatures and cooling agents like menthol induce cold sensation by activating the peripheral cold receptors TRPM8 and TRPA1, cation channels belonging to the TRP channel family, while the reduction of potassium currents provides an additional and/or synergistic mechanism of cold sensation. Despite extensive studies over the past decades to identify the molecular receptors that mediate thermosensation, cold sensation is still not fully understood and many cold-sensitive peripheral neurons do not express the well-established cold sensor TRPM8. We found that the voltage-gated potassium channel KCNQ1 (Kv7.1), which is defective in cardiac LQT1 syndrome, is, in addition to its known function in the heart, a highly relevant and sex-specific sensor of moderately cold temperatures. We found that KCNQ1 is expressed in skin and dorsal root ganglion neurons, is sensitive to menthol and cooling agents, and is highly sensitive to moderately cold temperatures, in a temperature range at which TRPM8 is not thermosensitive. C-fiber recordings from KCNQ1 -/- mice displayed altered action potential firing properties. Strikingly, only male KCNQ1 -/- is the first gene reported to play a role in sex-specific temperature sensation. Moreover, we propose that KCNQ1, together with TRPM8, is a key instrumentalist that orchestrates the range and intensity of cold sensation.TRPM8 -/- animals. While sex-dependent differences in thermal sensitivity have been well documented in humans and mice, KCNQ1 is the first gene reported to play a role in sex-specific temperature sensation. Moreover, we propose that KCNQ1, together with TRPM8, is a key instrumentalist that orchestrates the range and intensity of cold sensation., Competing Interests: Competing interests statement:The authors declare no competing interest.

Objective: The purpose of this study is to examine which rating scale is more suitable for objectivizing the subjective symptoms emphasized in Kampo clinical practice to ensure the high-quality of clinical evidence. Methods: A questionnaire survey on cold sensation was conducted in two groups of female students from the fourth year of T Medical University (in April and July) and a group of female patients who first visited the N Kampo Clinic. Three rating scales, descriptive question formats sometimes used in Kampo medicine, tentatively named "specific explanatory questions" (SEQs) in this study, verbal rating scale (VRS) with rating by qualitative words, and visual analogue scale (VAS) widely used to evaluate pain intensity were used for the questionnaire. Then we compared the evaluations of cold sensation and the effect of seasonal change in the environment among three scale methods, and difference in cold sensation by rating scale. Results: VRS was more able to properly evaluate the effect of change of seasons on cold sensation. Conclusion: VRS was considered to be more suitable as a rating scale for cold sensation evaluation because of these results, its wide acceptance in the field of psychology, and the ease with which VRS data can be processed statistically. [ABSTRACT FROM AUTHOR]

The detection of ambient cold is critical for mammals, who use this information to avoid tissue damage by cold and to maintain stable body temperature. The transduction of information about the environmental cold is mediated by cold-sensitive ion channels expressed in peripheral sensory nerve endings in the skin. Most transduction mechanisms for detecting temperature changes identified to date depend on transient receptor potential (TRP) ion channels. Mild cooling is detected by the menthol-sensitive TRPM8 ion channel, but how painful cold is detected remains unclear. The TRPA1 ion channel, which is activated by cold in expression systems, seemed to provide an answer to this question, but whether TRPA1 is activated by cold in neurons and contributes to the sensation of cold pain continues to be a matter of debate. Recent advances have been made in this area of investigation with the identification of several potential cold-sensitive ion channels in thermosensory neurons, including two-pore domain potassium channels (K2P), GluK2 glutamate receptors, and CNGA3 cyclic nucleotide-gated ion channels. This mini-review gives a brief overview of the way by which ion channels contribute to cold sensation, discusses the controversy around the cold-sensitivity of TRPA1, and provides an assessment of some recently-proposed novel cold-transduction mechanisms. Evidence for another unidentified cold-transduction mechanism is also presented.

The detection of ambient cold is critical for mammals, who use this information to avoid tissue damage by cold and to maintain stable body temperature. The transduction of information about the environmental cold is mediated by cold-sensitive ion channels expressed in peripheral sensory nerve endings in the skin. Most transduction mechanisms for detecting temperature changes identified to date depend on transient receptor potential (TRP) ion channels. Mild cooling is detected by the menthol-sensitive TRPM8 ion channel, but how painful cold is detected remains unclear. The TRPA1 ion channel, which is activated by cold in expression systems, seemed to provide an answer to this question, but whether TRPA1 is activated by cold in neurons and contributes to the sensation of cold pain continues to be a matter of debate. Recent advances have been made in this area of investigation with the identification of several potential cold-sensitive ion channels in thermosensory neurons, including two-pore domain potassium channels (K2P), GluK2 glutamate receptors, and CNGA3 cyclic nucleotide-gated ion channels. This mini-review gives a brief overview of the way by which ion channels contribute to cold sensation, discusses the controversy around the cold-sensitivity of TRPA1, and provides an assessment of some recently-proposed novel cold-transduction mechanisms. Evidence for another unidentified cold-transduction mechanism is also presented. [ABSTRACT FROM AUTHOR]

Background Thermal stimulation has been proposed as a modality to facilitate motor recovery in neurological populations, such as stroke. Recently (Ansari, Remaud & Tremblay, 2018), we showed that application of cold or warm stimuli distally to a single digit produced a variable and short lasting modulation in corticomotor excitability. Here, our goal was to extend these observations to determine whether an increase in stimulation area could elicit more consistent modulation. Methods Participants (n = 22) consisted of a subset who participated in our initial study. Participants were asked to come for a second testing session where the thermal protocol was repeated but with extending the stimulation area from single-digit (SD) to multi-digits (MD, four fingers, no thumb). As in the first session, skin temperature and motor evoked potentials (MEPs) elicited with transcranial magnetic stimulation were measured at baseline (BL, neutral gel pack at 22 °C), at 1 min during the cooling application (pre-cooled 10 °C gel pack) and 5 and 10 min post-cooling (PC5 and PC10). The analysis combined the data obtained previously with single-SD cooling (Ansari, Remaud & Tremblay, 2018) with those obtained here for MD cooling. Results At BL, participants exhibited comparable measures of resting corticomotor excitability between testing sessions. MD cooling induced similar reductions in skin temperature as those recorded with SD cooling with a peak decline at C1 of respectively, −11.0 and −10.3 °C. For MEPs, the primary analysis revealed no main effect attributable to the stimulation area. A secondary analysis of individual responses to MD cooling revealed that half of the participants exhibited delayed MEP facilitation (11/22), while the other half showed delayed inhibition (10/22); which was sustained in the post-cooling phase. More importantly, a correlation between variations in MEP amplitude recorded during the SD cooling session with those recorded in the second session with MD cooling, revealed a very good degree of correspondence between the two at the individual level. Conclusion These results indicate that increasing the cooling area in the distal hand, while still eliciting variable responses, did produce more sustained modulation in MEP amplitude in the post-cooling phase. Our results also highlight that responses to cooling in terms of either depression or facilitation of corticomotor excitability tend to be fairly consistent in a given individual with repeated applications.

Background: Thermal stimulation has been proposed as a modality to facilitate motor recovery in neurological populations, such as stroke. Recently (Ansari, Remaud & Tremblay, 2018), we showed that application of cold or warm stimuli distally to a single digit produced a variable and short lasting modulation in corticomotor excitability. Here, our goal was to extend these observations to determine whether an increase in stimulation area could elicit more consistent modulation. Methods: Participants (n = 22) consisted of a subset who participated in our initial study. Participants were asked to come for a second testing session where the thermal protocol was repeated but with extending the stimulation area from single-digit (SD) to multi-digits (MD, four fingers, no thumb). As in the first session, skin temperature and motor evoked potentials (MEPs) elicited with transcranial magnetic stimulation were measured at baseline (BL, neutral gel pack at 22 °C), at 1 min during the cooling application (pre-cooled 10 °C gel pack) and 5 and 10 min post-cooling (PC5 and PC10). The analysis combined the data obtained previously with single-SD cooling (Ansari, Remaud & Tremblay, 2018) with those obtained here for MD cooling. Results: At BL, participants exhibited comparable measures of resting corticomotor excitability between testing sessions. MD cooling induced similar reductions in skin temperature as those recorded with SD cooling with a peak decline at C1 of respectively, −11.0 and −10.3 °C. For MEPs, the primary analysis revealed no main effect attributable to the stimulation area. A secondary analysis of individual responses to MD cooling revealed that half of the participants exhibited delayed MEP facilitation (11/22), while the other half showed delayed inhibition (10/22); which was sustained in the post-cooling phase. More importantly, a correlation between variations in MEP amplitude recorded during the SD cooling session with those recorded in the second session with MD cooling, revealed a very good degree of correspondence between the two at the individual level. Conclusion: These results indicate that increasing the cooling area in the distal hand, while still eliciting variable responses, did produce more sustained modulation in MEP amplitude in the post-cooling phase. Our results also highlight that responses to cooling in terms of either depression or facilitation of corticomotor excitability tend to be fairly consistent in a given individual with repeated applications. [ABSTRACT FROM AUTHOR]

We hypothesized that menthol application on the skin would enhance vasoconstriction of subjects immersed in cool water, which would reduce heat loss and rectal temperature (Tre) cooling rate. Furthermore, it was hypothesized that this effect would be greater in individuals acclimatized to immersion in 24 °C water, such as swimmers. Seven swimmers ( SW) and seven physical education students ( CON) cycled at 60% VO2 max until Tre attained 38 °C, and were then immediately immersed in stirred water maintained at 24 °C on two occasions: without ( NM) and with (M; 4.6 g per 100 mL of water) whole-body skin application of menthol cream. Heart rate, Tre, proximal-distal skin temperature gradient, oxygen uptake ( VO2), electromyographic activity ( EMG), and thermal sensation were measured. Tre reduction was similar among SW and CON in NM and CON in M (−0.71±0.31 °C in average), while it was smaller for SW in M (−0.37±0.18 °C, P < 0.01). VO2 and heart rate were greater in M compared with NM condition ( P = 0.01). SW in M exhibited a shift of the threshold for shivering, as reflected in increased VO2 and EMG activity, toward a higher Tre compared with the other trials. Menthol application on the skin before immersion reduces heat loss, but defends Tre decline more effectively in swimmers than in non-swimmers. [ABSTRACT FROM AUTHOR]

To test the hypothesis that topical menthol-induced reactivity of cold sensation and cutaneous vasoconstriction to local cooling is augmented in individuals with a cold constitution, we examined thermal sensation and cutaneous vasoconstrictor responses at menthol-treated and untreated sites in the legs during local skin cooling in young women complaining of chilliness (C group) and young women with no complaint as a normal control group (N group). During local skin cooling, the sensitivity to cold sensation was greater in the C group than in the N group. The application of menthol enhanced the cold sensation at a low temperature in the N group, but not in the C group. Cutaneous vasoconstrictor responses to local skin cooling were not altered by menthol treatment in either of the two groups. These findings suggest the desensitization of menthol-activated cold receptors in the legs of C group subjects, and a minor role of cold receptor activity in cutaneous vasoconstrictor response to local cooling. [ABSTRACT FROM AUTHOR]

Copyright of Journal of the Japan Research Association for Textile End-Uses / Sen'i Seihin Shohi Kagaku is the property of Japan Research Association for Textile End-Uses / Sen'i Seihin Shohi Kagaku and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective Tarsal tunnel syndrome (TTS) is an entrapment neuropathy of the posterior tibial nerve in the tarsal tunnel. It is not known whether vascular or neuropathic factors are implicated in the cause of a cold sensation experienced by patients. Therefore, we studied the cold sensation in the pedal extremities of patients who did or did not undergo TTS surgery. Methods Our study population comprised 20 patients with TTS (38 feet); 1 foot was affected in 2 patients and both feet in 18 patients. We acquired the toe-brachial pressure index to evaluate perfusion of the sole and toe perfusion under 4 conditions: the at-rest position (condition 1); the at-rest position with compression of the foot dorsal artery (condition 2); the Kinoshita foot position (condition 3); and the Kinoshita foot position with foot dorsal artery compression (condition 4). Patients who reported abatement in the cold sensation during surgery underwent intraoperative reocclusion of the tibial artery to check for the return of the cold sensation. Results The toe-brachial pressure index for conditions 1 and 3 averaged 0.82 ± 0.09 and 0.81 ± 0.11, respectively; for conditions 2 and 4, it averaged 0.70 ± 0.11 and 0.71 ± 0.09, respectively. Among the 16 operated patients, the cold sensation in 7 feet improved intraoperatively; transient reocclusion of the tibial artery did not result in the reappearance of the cold sensation. Conclusions Our findings suggest that the cold sensation in the feet of our patients with TTS was associated with neuropathic rather than vascular factors. [ABSTRACT FROM AUTHOR]

To clarify the characteristics of the thermal control of skin blood flow (SkBF) in individuals with a cold constitution, we examined the cutaneous vasoconstrictor responses in the calf and dorsal foot during whole-body and local skin cooling in young women complaining of chilliness (C group) and young women not suffering from it (N group). During whole-body skin cooling, the vasoconstrictor sensitivity in the dorsal foot, but not in the calf, was greater in the C group than in the N group. The C group also showed greater vasoconstrictor responses in the dorsal foot, but not in the calf, during local skin cooling and the iontophoretic application of norepinephrine. These findings suggest that the C group possesses a specific SkBF controlling system that is characterized by higher adrenergic sensitivity for greater cutaneous vasoconstriction in the distal portion of the lower extremities during cold exposure. [ABSTRACT FROM AUTHOR]