Evaluating physiological strain during cold exposure using a new cold strain index. (1/364)

A cold strain index (CSI) based on core (T(core)) and mean skin temperatures (T(sk)) and capable of indicating cold strain in real time and analyzing existing databases has been developed. This index rates cold strain on a universal scale of 0-10 and is as follows: CSI = 6.67(T(core t) - T(core 0)). (35 - T(core 0))(-1) + 3.33(T(sk (t)) - T(sk 0)). (20 - T(sk 0))(-1), where T(core 0) and T(sk 0) are initial measurements and T(core t) and T(sk t) are simultaneous measurements taken at any time t; when T(core t) > T(core 0), then T(core t) - T(core 0) = 0. CSI was applied to three databases. The first database was obtained from nine men exposed to cold air (7 degrees C, 40% relative humidity) for 120 min during euhydration and two hypohydration conditions achieved by exercise-heat stress-induced sweating or by ingestion of furosemide 12 h before cold exposure. The second database was from eight men exposed to cold air (10 degrees C) immediately on completion of 61 days of strenuous outdoor military training, 48 h later, and after 109 days. The third database was from eight men repeatedly immersed in 20 degrees C water three times in 1 day and during control immersions. CSI significantly differentiated (P < 0.01) between the trials and individually categorized the strain of the subject for two of these three databases. This index has the potential to be widely accepted and used universally.  (+info)

Changes in cold-induced vasodilatation, pain and cold sensation in fingers caused by repeated finger cooling in a cool environment. (2/364)

To examine how repeated cooling of fingers with a rest pause schedule at work affects cold-induced vasodilatation (CIVD), pain and cold sensation in fingers, six healthy men aged 21 to 23 years immersed their left index fingers six times in stirred water at 10 degrees C for 10 minutes. After each cold-water immersion of the fingers, 5-minute rest pause was taken to observe the recovery process of the indicators. This cold-water immersion/rest pause test was carried out in a range of three ambient temperature conditions: 30 degrees C (warm), 25 degrees C (thermoneutral), and 20 degrees C (cool) as experienced in daily life. At the ambient temperatures of 30 degrees C and 25 degrees C, marked CIVD response occurred and the CIVD reactivity did not significantly change upon repetition of cold-water immersion. The lowered finger skin temperature also tended to recover quickly to the pre-immersion level during each post-immersion rest period. At the ambient temperature of 20 degrees C, however, the CIVD response weakened continuously upon repetition of immersion and almost disappeared during the final immersion. The recovery of finger skin temperature during each post-immersion rest was gradually delayed upon repetition of immersion. At every ambient temperature, finger pain and cold sensation induced by each cold-water immersion significantly decreased upon repetition of immersion and completely disappeared during each post-immersion rest period. Oral temperature during the experiment showed no significant change at the ambient temperatures of 25 degrees C and 30 degrees C, but it decreased significantly at the ambient temperature of 20 degrees C. These results suggest that in a cool work environment where the body core temperature is liable to decrease, repeated finger cooling may weaken CIVD reactivity and delay the recovery of finger temperature during post-immersion rest periods. In such lower ambient temperature work conditions, subjective judgements such as the decrease in finger pain and cold sensation during repeated finger cooling and the absence of them during post-immersion rest may not be reliable indicators for monitoring the risk of progressive tissue cooling and frostbite formation.  (+info)

Effect of ambient temperature on human pain and temperature perception. (3/364)

BACKGROUND: Animal studies show reduced nociceptive responses to noxious heat stimuli and increases in endogenous beta-endorphin levels in cold environments, suggesting that human pain perception may be dependent on ambient temperature. However, studies of changes in local skin temperature on human pain perception have yielded variable results. This study examines the effect of both warm and cool ambient temperature on the perception of noxious and innocuous mechanical and thermal stimuli. METHODS: Ten subjects (7 men and 3 women, aged 20-23 yr) used visual analog scales to rate the stimulus intensity, pain intensity, and unpleasantness of thermal (0-50 degrees C) and mechanical (1.2-28.9 g) stimuli applied on the volar forearm with a 1-cm2 contact thermode and von Frey filaments, respectively. Mean skin temperatures were measured throughout the experiment by infrared pyrometer. Each subject was tested in ambient temperatures of 15 degrees C (cool), 25 degrees C (neutral), and 35 degrees C (warm) on separate days, after a 30-min acclimation to the environment. Studies began in the morning after an 8-h fast. RESULTS: Mean skin temperature was altered by ambient temperature (cool room: 30.1 degrees C; neutral room: 33.4 degrees C; warm room: 34.5 degrees C; P < 0.0001). Ambient temperature affected both heat (44-50 degrees C) and cold (25-0 degrees C) perception (P < 0.01). Stimulus intensity ratings tended to be lower in the cool than in the neutral environment (P < 0.07) but were not different between the neutral and warm environments. Unpleasantness ratings revealed that cold stimuli were more unpleasant than hot stimuli in the cool room and that noxious heat stimuli were more unpleasant in a warm environment. Environmental temperature did not alter ratings of warm (37 and 40 degrees C) or mechanical stimuli. CONCLUSIONS: These results indicate that, in humans, a decrease in skin temperature following exposure to cool environments reduces thermal pain. Suppression of Adelta primary afferent cold fiber activity has been shown to increase cold pain produced by skin cooling. Our current findings may represent the reverse phenomenon, i.e., a reduction in thermal nociceptive transmission by the activation of Adelta cutaneous cold fibers.  (+info)

Thermal perception threshold testing for the evaluation of small sensory nerve fiber injury in patients with hand-arm vibration syndrome. (4/364)

The aim of the present study was to investigate whether thermal perception threshold testing is a useful method that could replace pain threshold testing in the evaluation of small sensory nerve fiber injury in vibration-induced neuropathy. Vibration, pain, and thermal (warm and cold) perception thresholds were examined on both middle fingers of 50 patients with hand-arm vibration syndrome and 29 healthy controls of similar age. The patients were divided into three subgroups according to the Stockholm Workshop sensorineural scale. Thermal (warm and cold) thresholds as well as vibration and pain thresholds were significantly more deteriorated among the patients than in the controls. Among the patients, warm thresholds elevated and cold thresholds lowered according to the Stockholm Workshop scale. Thermal thresholds were significantly correlated with pain thresholds, and the sensitivity of the thermal threshold testing tended to be greater than that of the pain threshold testing. The present findings indicate that thermal threshold testing for warm and cold perception can be a useful substitute for pain threshold testing to examine small nerve fiber injury in vibration-induced neuropathy.  (+info)

Restricted dissociated sensory loss in a patient with a lateral medullary syndrome: A clinical-MRI study. (5/364)

BACKGROUND: Various sensory syndromes in lateral medullary infarctions are described. A small variation in the location of a lesion may lead to very different clinical features, owing to the complex anatomy of the medulla oblongata. MRI may identify the location and extent of the ischemic lesions, allowing a clear clinical-anatomical correlation. CASE DESCRIPTION: We describe a man with an ischemic lesion in the right portion of the lower medulla that presented a contralateral impairment of spinothalamic sensory modalities and an ipsilateral impairment of lemniscal modalities with a restricted distribution (left forearm and hand, right hand and fingers, respectively). The restricted and dissociated sensory abnormalities represent the only permanent neurological consequence of that lesion. CONCLUSIONS: The atypical sensory syndrome may be explained by the involvement of the medial portion of spinothalamic tract and the lateral portion of archiform fibers at the level of the lemniscal decussation.  (+info)

Habituation of thermal sensations, skin temperatures, and norepinephrine in men exposed to cold air. (6/364)

We studied habituation processes by exposing six healthy men to cold air (2 h in a 10 degrees C room) daily for 11 days. During the repeated cold exposures, the general cold sensations and those of hand and foot became habituated so that they were already significantly less intense after the first exposure and remained habituated to the end of the experiment. The decreases in skin temperatures and increases in systolic blood pressure became habituated after four to six exposures, but their habituations occurred only at a few time points during the 120-min cold exposure and vanished by the end of the exposures. Serum thyroid-stimulating hormone, total thyroxine and triiodothyronine, norepinephrine, epinephrine, cortisol, and total proteins were measured before and after the 120-min cold exposure on days 0, 5, and 10. The increase in norepinephrine response became reduced on days 5 and 10 and that of proteins on day 10, suggesting that the sympathetic nervous system became habituated and hemoconcentration became attenuated. Thus repeated cold-air exposures lead to habituations of cold sensation and norepinephrine response and to attenuation of hemoconcentration, which provide certain benefits to those humans who have to stay and work in cold environments.  (+info)

Redistribution of sudomotor responses is an early sign of sympathetic dysfunction in type 1 diabetes. (7/364)

Patients with diabetic neuropathy typically have decreased sweating in the feet but excessive sweating in the upper body. Previous studies of sudomotor function in diabetes have included patients with longstanding disease. The present study was designed to test for the early presence of sudomotor dysfunction and to characterize its relation to glycemic control and other aspects of peripheral nerve function. A total of 37 patients (10 males, 27 females) enrolled in a longitudinal study, in which autonomic function was evaluated annually for 3 years. Patients enrolled 2-22 months after the diagnosis of type 1 diabetes. Forty-one age- and sex-matched healthy control subjects were also studied. Sweat production in response to acetylcholine stimulation was dramatically increased in the forearm at the time of the first evaluation (1.67 +/- 0.24 micro/cm2 in the diabetic patients vs. 1.04 +/- 0.14 microl/cm2 in the control subjects, P < 0.05). Likewise, the ratio of sweating in the forearm to sweating below the waist was higher in the diabetic patients (0.553 +/- 0.07 microl/cm2) than in the control subjects (0.385 +/- 0.04 microl/cm2, P < 0.05). Forearm sweat was negatively associated with the renin-toprorenin ratio and vanillylmandelic acid (VMA) excretion (P < 0.025), tests of sympathetic nerve function. The ratio of sweating in the forearm to sweating in the foot was likewise increased in diabetic patients with poor glycemic control. We interpret this redistribution of sudomotor responses to be indicative of sympathetic nerve injury and conclude 1) that the sympathetic nervous system is especially vulnerable to the adverse effects of chronic hyperglycemia and 2) that sympathetic dysfunction can be detected very early in type 1 diabetes.  (+info)

Ca2+ signaling via the neuronal calcium sensor-1 regulates associative learning and memory in C. elegans. (8/364)

On a radial temperature gradient, C. elegans worms migrate, after conditioning with food, toward their cultivation temperature and move along this isotherm. This experience-dependent behavior is called isothermal tracking (IT). Here we show that the neuron-specific calcium sensor-1 (NCS-1) is essential for optimal IT. ncs-1 knockout animals show major defects in IT behavior, although their chemotactic, locomotor, and thermal avoidance behaviors are normal. The knockout phenotype can be rescued by reintroducing wild-type NCS-1 into the AIY interneuron, a key component of the thermotaxis network. A loss-of-function form of NCS-1 incapable of binding calcium does not restore IT, whereas NCS-1 overexpression enhances IT performance levels, accelerates learning (faster acquisition), and produces a memory with slower extinction. Thus, proper calcium signaling via NCS-1 defines a novel pathway essential for associative learning and memory.  (+info)