A student nurse intervenes to foster grandfather/grandchild bonding.

This article describes the important role played by a student nurse in assisting a new grandparent bond with his granddaughter. This grandfather had been a noncustodial parent to his daughter, and as such, was anxious about his new role. The increasing numbers of noncustodial parents becoming grandparents presents a new problem facing nurses in helping a family meet their new members. The opportunity for grandparent/grandchild bonding may be enhanced by nurses who are sensitive to the less-than-perfect relationship that might exist between a noncustodial parent and the adult child. These grandparents may need encouragement to find their place in the life of the new child.

Use of a mental rotation reaction-time paradigm to measure the effects of upper cervical adjustments on cortical processing: a pilot study.

OBJECTIVES: To investigate the potential usefulness of a mental rotation paradigm in providing an objective measure of spinal manipulative therapy. To determine if cortical processing, as indicated by response time to a mental rotation reaction-time task, is altered by an upper cervical toggle recoil adjustment. DESIGN: Prospective, double-blind, randomized, controlled trial. SETTING: Chiropractic college clinical training facility. PARTICIPANTS: Thirty-six chiropractic student volunteers with clinical evidence of upper cervical joint dysfunction. INTERVENTION: Participants in the experimental group received a high-velocity, low-amplitude upper cervical adjustment. A non-intervention group was used to control for improvement in the mental rotation task as a result of practice effects. OUTCOME MEASURES: Reaction time was measured for randomly varying angular orientations of an object appearing either as normal or mirror-reversed on a computer screen. RESULTS: The average decrease in mental rotation reaction time for the experimental group was 98 ms, a 14.9% improvement, whereas the average decrease in mental rotation reaction time for the control group was 58 ms, an 8. 0 improvement. The difference scores after the intervention time were significantly greater for the experimental group compared with the control group, as indicated by a one-tailed, 2-sample, equal variance Student t test, (P < 05). CONCLUSION: The results of this study have demonstrated a significant improvement in a complex reaction-time task after an upper cervical adjustment. These results provide evidence that upper cervical adjustment may affect cortical processing.

Chromosomes and stress.

The present investigation examines genotoxic effects of: prolonged periods of stress; the role of the endocrine system; and the relationship between psychogenic stress and chemical mutagens. Increased levels of both Sister Chromatid Exchanges (SCEs) and Chromosome Aberrations (CAs) were observed in male rats subjected to white noise of either 72 or 240 hrs duration, demonstrating that damage occurs during chronic stress. Rats subjected to foot-shock after having been either hypophysectomized or sham-operated, showed elevation of both SCEs and CAs, indicating that hormones in the hypothalamic-pituitary-adrenal axis do not play a role in genotoxic damage. Rats subjected to foot-shock, and/or the mutagen Mitomycin-C(MMC) showed elevated SCEs, both separately and together. The combined effect was the sum of the individual effects, demonstrating that synergism was not involved. This investigation establishes that psychogenic stress plays a role in genotoxic damage.

Psychogenic stress induces chromosomal and DNA damage.

In this investigation, rats subjected to swim stress showed within 24 hours significant increases in both the level of chromosome aberrations and Sister Chromatid Exchanges (SCEs) in bone marrow cells. The generality of cytogenetic damage by behavioral stressors was demonstrated by exposing rats to both cold-and warm-water forced swims, to white noise, and to continuous or intermittent inescapable foot shock stress (IFS). The induction of chromosome aberrations and SCEs, to differing degrees, by stressors that differ both quantitatively and qualitatively, demonstrates that this is a general phenomenon of stress. The use of an additional measure, unscheduled DNA Synthesis (UDS) showed that stress-induced genotoxic damage can occur in a second cell type and on a molecular as well as chromosomal level. These results indicate that there may be a cellular genetic basis for some of the effects of stress.

Characterization of pituitary mediation of stress-induced antinociception in rats.

Antinociception, induced by continuous cold-water swims (CCWS) and certain parameters of inescapable foot shock, is reduced in hypophysectomized rats receiving supplements of corticosterone and l-thyroxine. To assess which lobe of the pituitary gland is involved in this effect, the first experiment compared the effects of total hypophysectomy and posterior lobectomy in supplemented rats upon CCWS antinociception on the tail-flick and jump tests and upon continuous inescapable foot shock antinociception on the tail-flick test. Total hypophysectomy, but not posterior lobectomy, significantly reduced CCWS antinociception on both tests in supplemented rats relative to sham surgery. Both total and posterior hypophysectomy either reduced or potentiated foot shock antinociception as functions of shock intensity or duration of exposure in supplemented rats. To assess whether hormonal supplementation is necessary for the observed effects, the second experiment examined CCWS antinociception in sham-operated and hypophysectomized rats that received either no hormonal supplements or corticosterone and/or l-thyroxine. These regimens failed to alter CCWS antinociception in sham-operated rats. Treatment of hypophysectomized rats with corticosterone and l-thyroxine either separately or together significantly reduced CCWS antinociception. In contrast, if hypophysectomized rats did not receive supplements, CCWS antinociception was significantly potentiated relative to sham-operated controls. These effects could not be attributed to treatment-induced changes in either body weight or CCWS hypothermia. These data suggest that the anterior lobe of the pituitary gland and adrenal cortex are involved in the mediation and/or maintenance of CCWS antinociception.

Sister chromatid exchanges induced by behavioral stress.

Rats subjected to swim stress showed a doubling of sister chromatid exchange (SCE) level. In a second experiment, the generality of SCE induction by behavioral stressors was tested by exposing rats to either swim, white noise, or either continuous or intermittent inescapable footshock stress. The induction of SCEs, although to differing degrees, by qualitatively different stressors, demonstrates that this is a general phenomenon of stress. There may be a cellular genetic basis for some of the effects of stress.

Potentiation of cold swim stress analgesia in rats by diazepam.

It was hypothesized that diazepam (DZP) would attenuate the analgesia produced by cold swim stress because of its anxiolytic and biochemical anti-stress properties. In fact, it had the opposite effect. Administered alone, neither DZP nor its vehicle affected the nociceptive thresholds of rats, as assessed by a flinch-jump test. In combination with cold swim stress, DZP elevated nociceptive thresholds significantly more than did the stressor alone. This was true whether DZP was injected before or after exposure to the stressor, or whether or not DZP administration was acute or chronic.

Constraints on the tailflick assay: morphine analgesia and tolerance are dependent upon locus of tail stimulation.

In three experiments, the locus of tail stimulation in the tailflick assay was found to be an important parameter in determining morphine action. Rats were intravenously infused (Experiment I), injected with morphine subcutaneously (Experiment II), or implanted subcutaneously with morphine pellets (Experiment III). Analgesia was evaluated periodically following drug administration using the tailflick test and 3 adjacent 1 in. tail areas. In all three experiments, the distal tail section was more sensitive to the analgesic effects of morphine than more proximal sections. In Experiments I and III, tolerance to the effects of morphine developed more slowly at the distal tail location. These results indicate that the locus of stimulation in the tailflick assay can profoundly affect the development of analgesia and tolerance to morphine.

The role of endorphins in stress-induced analgesia.

We have seen that exposure of an organism to any of a wide range of stressful situations can induce alterations in sensitivity to pain that outlast the exposure. Not all stressors induce analgesia; among those that do not are some that produce maximal elevations in plasma beta-endorphin, ACTH, and adrenal corticosteroids. Some examples of SIA are sensitive to opiate receptor blockade by naloxone, but others are not. Hypophysectomy produces a similarly uneven profile of effects across different stressors. This diversity has often been interpreted as evidence for the existence of an array of pain inhibitory systems, with differing physiological properties and activated by different stressors. However, it might also suggest that stressors can prompt a variety of behavioral changes, many of which can be interpreted as analgesia if a pain reflex test is employed as the dependent measure.

Reversal of stress-induced analgesia by apomorphine, but not by amphetamine.

Acute exposure to severe stressors induce profound analgesia as well as depleting catecholamine levels. The present study examined whether d-amphetamine and apomorphine, agents which increase catecholamine availability, would alter the analgesic effectiveness of cold-water swims (CWS) and 2-deoxy-D-glucose (2-DG) as measured by an operant liminal escape procedure. Two groups of 10 rats each were tested to determine alterations in liminal escape threshold functions following amphetamine at doses of 0.25, 0.5, 1, 2 mg/kg and following apomorphine at doses of 0.025, 0.05, 0.1, 0.2 mg/kg. Half of the amphetamine and half of the apomorphine groups were tested across their respective dose ranges for the drug effects upon CWS analgesia. The remaining animals in each group received 2-DG (600 mg/kg IP) alone followed by 2-DG paired with each stimulant dose. No dose of amphetamine or apomorphine alone altered escape thresholds. While amphetamine produced slight potentiations of 2-DG analgesia at the two low doses, apomorphine at the 0.05 and 0.1 mg/kg doses returned CWS and 2-DG analgesia to within normal placebo values. These results provide indirect evidence for a role for brain norepinephrine and dopamine in stress-induced analgesia, and these data are discussed with respect to catecholamine involvement in pain-inhibitory processes.

Enhancement of conditioned autonomic responses in monkey when preshock signals occasion operant suppression.

Classical pairings of a sound stilulus with shock elicited larger magnitude and more rapidly conditioned autonomic responses when subjects were responding on variable-interval schedules for food than when they were eating freely available food. The difference was not attributable to changes in control values of heart rate and blood pressure, or to alterations in motor activity, but appeared related to operant suppression.

Stress-induced analgesia: neural and hormonal determinants.

Extensive evidence has indicated that distinct neural systems specifically designed to inhibit sensitivity to painful stimuli exist. Recent advances suggest that the endorphins, enkephalins and the opiate receptor interact with a descending serotonergic bulbospinal system to mediate the analgesic responses to opiates and electrical stimulation. In assessing the evolutionary and behavioral significance of this pain-inhibitory system, several laboratories discovered that acute exposure to a wide variety of stressful events results in a transient analgesia. Chronic exposure to a number of these stressors results in adaptation of the analgesic response. The purpose of this review is to identify and characterize the mechanisms by which these stressors activate pain-inhibition. The relationship of stress-induced analgesia to each of the following is reviewed: (a) the role of endorphins, enkephalins and the opiate receptor; (b) the role of the descending serotonergic bulbospinal system; (c) the role of the pituitary gland; and (d) the role of hypothalamic mechanisms. Data will be discussed in terms of "opiate" and "non-opiate" pain-inhibitory mechanisms, in which some stressors act through the former and other stressors act through the latter.

Chlordiazepoxide antinociception: cross-tolerance with opiates and with stress.

Chlordiazepoxide (CDP) has been previously shown to possess antinociceptive properties that are resistant, except at high doses, to the opiate antagonist naloxone. The present study evaluated whether CDP's antinociceptive effects were subject to tolerance following repeated injections and whether cross-tolerance might develop between the antinociceptive action of CDP and that of either morphine or cold water swins. CDP increased flinch-jump thresholds following acute administration and exhibited tolerance following repeated injections. Neither morphine-tolerant nor cold water swim-adapted rats displayed an antinociceptive effect when tested with CDP. On the other hand, chronic pretreatment with CDP attenuated the antinociceptive effects of cold water swims, but did not produce any clear effect upon morphine analgesia.

2-Deoxy-D-glucose analgesia: influences of opiate and non-opiate factors.

Acute administration of 2-deoxy-D-glucose (2-DG), an antimetabolic glucose analogue induces a powerful analgesia which adapts following repeated administration. 2-DG analgesia displays significant cross-tolerance with morphine, and like morphine analgesia, is potentiated in hypophysectomized rats. The present study examined further the role of opiates in 2-DG analgesia by examining whether the opiate antagonist, naloxone, would affect 2-DG analgesia, and whether ineffective doses of 2-DG and morphine would interact in a synergistic fashion to induce analgesia. Nociceptive thresholds were measured by the flinch-jump test. Naloxone doses of 1, 5, 10 and 20 mg/kg were all ineffective in reducing significantly 2-DG (600 mg/kg) induced pain threshold elevations. Naloxone failed to attenuate 2-DG (350 mg/kg) analgesia whether administered before or after the 2-DG injection. On the other hand, simultaneous administration of sub-analgesic doses of 2-DG (200 mg/kg) and morphine (2.5 mg/kg) summated to produce significant analgesia. This, 2-DG analgesia is similar to opiates in its tolerant and summative actions, yet dissimilar in that naloxone is ineffective in reversing its effects.

Differential effects of hypophysectomy upon analgesia induced by two glucoprivic stressors and morphine.

Pain threshold elevations induced in rats following acute exposure to stressful cold-water swims and to inescapable foot shocks are significantly attenuated by hypophysectomy. The present study investigated the effects of hypophysectomy upon the dose-dependent and time-dependent analgesia induced by morphine and by the glucoprivic agents, 2-deoxy-D-glucose (2-DG) and insulin. Two reflex pain tests, the tail-pinch and the flinch-jump were employed. In normal rats, insulin induced prolonged (180 min) analgesia at doses of 16 U/kg on the tail-pinch test and 256 U/kg on the flinch-jump test. However, the same agents induced small and brief pain threshold elevations in hypophysectomized animals. By contrast, though 2-DG increased both measures in both groups, its effects were more marked in hypophysectomized rats. Hypophysectomized rats also exhibited a potentiated analgesic effect on both tests following high doses of morphine. On the other hand, low doses of morphine transiently increased tail-pinch thresholds in normal, but not hypophysectomized subjects. These data provide further evidence of multiple pain-inhibitory mechanisms in which the pituitary plays a complex, but integral part.

Analgesia induced by cold-water stress: attenuation following hypophysectomy.

In addition to the well-known activation of the pituitary-adrenal axis, acute exposure to severe stressors includes a temporary analgesia in rats. Thus, the present study investigates whether the pituitary was involved in the mediation of analgesia induced by severe cold-water swim (CWS) stress. Flinch-jump thresholds were measured 30 min following 3.5-min swims in water temperatures ranging from 2-35 degrees C. Compared with untreated normal rats, hypophysectomized rats, receiving corticosterone and thyroxin, displayed significantly less CWS-induced analgesia, while similarly-supplemented normal rats exhibited significantly more CWS-induced analgesia. In a second experiment, operant liminal escape pain thresholds were determined following acute and chronic CWS. Whereas normal rats exhibited profound analgesia following the initial swims, the hypophysectomized rats never displayed any CWS-induced operant escape shifts. Stress-induced alterations in general activity levels and/or thermoregulation were shown to be unrelated to the diminished effectiveness of CNS to produce analgesia in hypophysectomized rats. These data imply that the pituitary is involved in the mediation of CWS-induced analgesia.