Rest-Activity Rhythm, Pain, and Motor Activity in Multiple Sclerosis.

BACKGROUND: Although the relationships among physical disability, mood disorders, and pain are well described in multiple sclerosis (MS), little is known about whether those symptoms are associated with sleep disturbances. METHODS: Forty-six patients with MS experiencing pain participated. Sleep was indirectly measured by assessing rest-activity rhythm via actigraphy: interdaily stability, intradaily variability, and relative amplitude. Pain was assessed using visual and verbal analog scales, mood by the Beck Depression Inventory and Symptom Checklist-90, and physical disability by the Expanded Disability Status Scale. RESULTS: Incorporating mood, pain, and physical disability into 1 regression model resulted in a significant association with interdaily stability. CONCLUSIONS: Compared with intradaily variability and relative amplitude, interdaily stability seems to be the most vulnerable actigraphy variable for mood disturbances, pain, and physical disabilities.

Patterns of body temperature during feeding in rats under varying ambient temperatures.

Relationships between feeding and body temperature of rats were investigated at three ambient temperatures during the whole light/dark cycle. Basal liver temperature was negatively correlated with ambient temperature. Only at 29 degrees C liver temperature indicated activation of autonomic and locomotory thermoregulatory responses due to heat stress. At 21 degrees C, liver temperature was always higher than skin temperature. Both showed a clear circadian rhythm with higher values during the dark phase. Meal-associated temperature patterns were superimposed on this circadian rhythm. Liver and skin temperatures showed a preprandial and prandial rise. Liver temperature reached an almost similar peak value just above 39 degrees C at the end of a meal, irrespective of meal size and ambient temperatures of 13 degrees C and 21 degrees C. Liver temperature reached this peak about 2 min earlier and dropped sooner than skin temperature. These results indicate a threshold liver temperature at which feeding activity stops. The present study suggests that temperatures do not exceed this value by adaptive autonomic thermoregulatory responses shifting heat flow from core to skin and by stopping all locomotory activities including feeding, thereby avoiding deterioration of vital organs and physiological processes due to hyperthermia.

Age-related alterations in cardiac response to emotional stress: relations to behavioral reactivity in the rat.

Age and behavioral characteristics are considered as risk factors for disturbances of the cardiac rhythm. Emotional stress may be a disseminating factor. Therefore, cardiac responsiveness and behavioral reactivity and their relation as a function of age have been studied in the rat. Young (3-month-old) and young adult (5-month-old) rats display a relative deceleratory cardiac response with bradyarrhythmias in the initial phase of response to emotional stress evoked by stimuli associated with a previous painful experience. The behavioral response is immobility. The immobility response is also displayed by aged (21-month-old) and senescent (33-month-old) rats but the initial bradycardiac heart response to emotional stress is absent, and the incidence of repetitive extrasystoles is increasing with age. An inverse correlation between behavioral reactivity to novel stimuli and the bradycardiac heart responsiveness is observed in young and young adult individual animals. The behavioral reactivity of the aged and senescent rats is diminished, but the correlation with cardiac reactivity remains preserved. It is suggested that the behaviorally coupled inhibitory influences on the heart are diminishing during aging either due to impairments in the descending cholinergic (vagal) system or secondarily, due to a decrease in the central "drive" of this system.

Hepatic-portal and cardiac infusion of CCK-8 and glucagon induce different effects on feeding.

In order to compare effects of circulating CCK-8 and glucagon on food intake, rats were provided with a permanently implanted catheter in the right atrium. Another cannula was implanted into the hepatic-portal vein by a new technique. After a standard fasting period graded loads of CCK-8 and glucagon were infused via these catheters during refeeding. Intracardiac glucagon and CCK loads dose-dependently suppressed meal size. Intraportal infusion of glucagon caused similar suppression compared to intracardiac administration. This may indicate a minor role of the liver as a target for the suppression of feeding by glucagon. In contrast, intraportal infusion of CCK-8 did not reduce food intake. The results indicate that CCK-8 is removed or inactivated by the liver. It is suggested that CCK-8 acts locally on vagal nerve endings to exert its suppressive action on food intake.

Daily variation of food-induced changes in blood glucose and insulin in the rat and the control by the suprachiasmatic nucleus and the vagus nerve.

Rats were provided with permanent cardiac catheters allowing free movement and blood sampling without anaesthesia. During food intake the increments of plasma insulin and blood glucose were smaller and more slowly increasing in the light phase than during the dark phase. After vagal blockade the increase in both blood glucose and plasma insulin was reduced. Since this effect was more prominent in the dark phase it suggests that during this phase vagal activity may stimulate an increase in glucose inflow into the blood by activating transport and digestion of food. Electrolytic lesions of the nucleus suprachiasmaticus caused disappearance of the circadian variation of insulin and glucose responses. In this situation in both phases rapid increments of insulin and glucose occurred similar to the controls during the dark phase. It is suggested that the nucleus suprachiasmaticus directly or indirectly controls vagal activity, which determines via its influence on the gastrointestinal tract the circadian variation in blood glucose and plasma insulin responses after food intake.

Interaction between circadian and caloric control of feeding behavior in the rat.

Feeding at the beginning of the night is probably dependent on the rat's immediate energy requirements while feeding at the end may have an anticipatory function. This latter feeding peak may be mainly controlled by a circadian pacemaker. The aim of this study was to investigate the relative contribution of satiety signals and circadian pacemakers in the control of feeding behavior. Food intake was monitored after infusion of liquid food into the stomach during several parts of the day-night cycle to prevent a possible influence of oral sensations. It is demonstrated that intragastric infusion is more effective in suppressing intake during daytime and the first half of the dark phase than during the second half of the dark phase. Suppressions of food intake are mainly due to delaying the first occurrence of food ingestion, whereas the size of that meal is less affected. During the last period of the night no significant delay could be brought about. These experiments suggest that in the rat a circadian pacemaker dominates feeding motivation during the end of the night thereby strongly interacting with caloric control of feeding behavior.

Effect of skeleton photoperiod and food availability on the circadian pattern of feeding and drinking in rats.

Feeding and drinking behavior were measured in rats maintained under a 12:12 light-dark (LD) cycle or skeleton photoperiod (SPP). Feeding and drinking were closely associated during the normal LD cycle but under SPP conditions an increased feeding activity during the subjective day was not accompanied by an equivalent increment of water intake. This indicates a stronger coupling of drinking to the subjective night. A restriction of food availability to the subjective light phase did not cause an accompanying complete shift in drinking behavior. These results suggest that drinking is largely dependent on the influence of a circadian oscillator and this association is not disrupted by changes in feeding schedule. A change in food access to the subjective light phase caused partial but not permanent desynchronization between feeding and drinking behavior. Synchrony was reestablished within one day once food was available ad lib. Complete return to the original feeding and drinking patterning took 3 days. It is suggested that separate slave oscillators controlling feeding and drinking are governed by a hypothesized "master" circadian oscillator which remains definitely entrained to the original rhythm by the light pulses of the SPP condition.

Reduced insulin secretion after short-term food deprivation in rats plays a key role in the adaptive interaction of glucose and free fatty acid utilization.

The present study was undertaken to investigate the effects of short-term fasting periods up to 24 hr on insulin secretory responses of the B-cell to glucose and the consequences for FFA and glucose availability in the circulation. Conscious male rats provided with permanently implanted heart catheters received glucose infusions at midday, lasting for 20 min, in the nearly ad lib condition (i.e., 6 hr of non feeding during daytime) and after extending the fasting period to 12, 18 and 24 hr. Basal preinfusion insulin levels and insulin responses to glucose decreased gradually during these fasting periods. Basal blood glucose dropped only significantly after 24 hr of fasting whereas basal FFA levels increased gradually from 6 hr of fasting onwards. After prolonged fasting insulin released during glucose infusion became more effective in suppressing plasma FFA levels. While our data suggest that the sensitivity to the antilipolytic action of insulin is increased, the decreased responsiveness of the B-cell after moderate fasting periods may result in a drop of basal insulin levels. This facilitates the switch from glucose to FFA metabolism for most tissues already, when the first meals are missed. The results suggest that this physiological process is important to save the glycogen stores as long as possible as fuel for the central nervous system, and also to support basic energy requiring processes adequately.