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Stress radionuclide myocardial perfusion imaging detects more residual ischemia than stress echocardiography following acute myocardial infarction.

OBJECTIVES: This investigation sought to compare the abilities of stress radionuclide myocardial perfusion imaging and stress echocardiography to detect residual ischemia in patients following acute myocardial infarction (MI). BACKGROUND: Stress radionuclide myocardial perfusion imaging and stress echocardiography are both commonly used to assess patients (patients.) in the immediate post MI period. However, the relative value of these techniques in identifying post MI ischemia remains unclear. METHODS: Eighteen patients. underwent both dipyridamole radionuclide perfusion imaging and dobutamine stress echocardiography on the same day or on consecutive days, 3-7 days following uncomplicated acute MI. Pts. who had an acute percutaneous intervention were excluded. Images were reviewed with clinical information available, but blinded to the opposing modality, for perfusion defects, wall motion abnormalities (WMA), and evidence of ischemia (reversible defect(s) on perfusion imaging, worsening WMA on stress echocardiography). Of the 18 patients, 11 subsequently underwent cardiac catheterization. RESULTS: Perfusion imaging identified defects in 16 (89%) patients, of whom 15 (83% of total) were found to be ischemic. Stress echocardiography identified a fixed wall motion abnormality in 17 (94%) and ischemia in 8 (44%, p < 0.05 compared with perfusion imaging ischemia). Among 11 patients who underwent catheterization, there was a trend towards perfusion imaging identifying more ischemia in the territory of an obstructed (> or = 70%) vessel--100% (11/11) vs. 64% (7/11) for stress echocardiography (p = 0.09). CONCLUSION: In the immediate post-infarction period, dipyridamole stress radionuclide myocardial perfusion imaging more often shows evidence of residual ischemia than dobutamine stress echocardiography.

Adult↗

[Stress reactions--stress fracture of the upper femoral neck in endurance sports].

Stress reactions of the musculoskeletal system may be interpreted as possible precursors of stress fractures. Biological material, in contrast to artificial products, can react in numerous and complex ways. This can not only lead to a continual weakening of the tissue, but also to adaptation phenomena in response to overuse. The causes of such stress reactions are still unclear in many respects. For example, it is unknown to what extent a predisposition to these stress symptoms is created by mechanical stress alone or whether other factors such as physical condition, nutrition or even hormone balance come into play. Early diagnosis considerably reduces the healing process and, the later the diagnosis of the stress reaction, the more drawn out is the healing process and the extent of the athlete's absence from training. In this connection may be discussed whether the stress reaction can be the represent as the precursor of the stress fracture. In light of the need for taking special care in obtaining anamnestic data and determining the predisposition of an athlete, it appears to be justified to perform whole body bone scanning in the initial stages and particularly after an innocuous radiological finding. To what extent more current methods (e. g. MRI) can be applied without exposing the athlete to undue radiation cannot be conclusively judged at present. The treatment of a stress reaction should, at least at the beginning, be the same as for a diagnosed stress fracture.

Adult↗

Interactive relationships between hospital patients' noise-induced stress and other stress with sleep.

OBJECTIVE: The purpose of this study was to test the hypothesis that hospital noise-induced subjective stress would interact with other subjective environmental and personal stress in a relationship with poorer patient sleep. METHODS: A secondary data analysis was done using correlations and hierarchical multiple regression. Ninety-seven cardiac patients participated after transfer from critical care to a general unit. The independent variables were assessed with Topf's 24-item Disturbance Due to Hospital Noise Scale and 5-point items for other environmental stress (ie, bed, lights) and personal stress (ie, pain, anxiety). Sleep was evaluated with the Verran and Snyder-Halpern Sleep Scale. RESULTS: Hierarchical multiple regression led to a multiple R of 0.435 (P <.01). An interaction term, subjective noise stress x subjective bed stress x subjective pain x subjective anxiety accounted for a significant amount of sleep variance (12%, F = 13.63, P =.000). Subjective bed stress x subjective pain accounted for an additional 5% (F = 6.4, P =.013). CONCLUSIONS: Studies using research designs that assess relationships between multiple patient stress variable interactions and sleep or other stress-related outcomes may produce more accurate results than studies on the independent effects of different types of stress.

Adult↗

Physiological roles of ASK1-mediated signal transduction in oxidative stress- and endoplasmic reticulum stress-induced apoptosis: advanced findings from ASK1 knockout mice.

Apoptosis, a molecularly regulated form of cell death, is essential for the normal functioning and homeostasis of most multicellular organisms, and can be induced by a range of environmental, physical, and chemical stresses. As the cellular decision to live or to die is made by the coordinated action and balancing of many different pro- and antiapoptotic factors, defects in control of this coordination and balance may contribute to a variety of human diseases, including cancer and autoimmune and neurodegenerative conditions. In recent years, multiple factors associated with the execution of apoptosis, such as caspases and Bcl-2 family members, have been discovered and their complicated signaling and molecular interactions have been demonstrated; however, the precise mechanistic basis for intracellular and/or extracellular stress-induced apoptosis remains to be fully characterized. Protein kinases contribute to regulation of life and death decisions made in response to various stress signals, and the actions of pro- and antiapoptotic factors are often affected by modulation of the phosphorylation status of key elements in the execution of apoptosis. Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein (MAP) kinase kinase kinase family, which activates both the MKK4/MKK7-JNK and MKK3/MKK6-p38 MAP kinase pathways and constitutes a pivotal signaling pathway in various types of stress-induced apoptosis. We have recently shown through ASK1 gene ablation in mice that ASK1 plays essential roles in oxidative stress- and endoplasmic reticulum (ER) stress-induced apoptosis. These stresses are closely linked to physiological phenomena in the control of cell fate, and the resultant apoptosis is implicated in the pathophysiology of a broad range of human diseases. This article reviews our new findings on the physiological roles of ASK1-mediated signal transduction in stress responses and the molecular mechanisms by which ASK1 determines cell fate such as survival, differentiation, or apoptosis, with special focus on the regulatory mechanisms of ASK1-mediated apoptosis induced by oxidative stress and ER stress.

Animals↗

The DSCR1 (Adapt78) isoform 1 protein calcipressin 1 inhibits calcineurin and protects against acute calcium-mediated stress damage, including transient oxidative stress.

Although DSCR1 (Adapt78) has been associated with successful adaptation to oxidative stress and calcium stress and with devastating diseases such as Alzheimer's and Down syndrome, no rationale for these apparently contradictory findings has been tested. In fact, DSCR1 (Adapt78) has not yet been proved to provide protection against acute oxidative stress or calcium stress. We have addressed this question using cross-adaptation to H2O2 and the calcium ionophore A23187, stable DSCR1 (Adapt78) transfection and overexpression in hamster HA-1 cells, 'tet-off' regulated DSCR1 (Adapt78) isoform 1 transgene expression in human PC-12 cells, and DSCR1 (Adapt78) antisense oligonucleotides to test the ability of the DSCR1 (Adapt78) protein product calcipressin 1 (a calcineurin inhibitor) to protect against oxidative stress and calcium stress. Under all conditions, resistance to oxidative stress and calcium stress increased as a function of DSCR1 (Adapt78)/calcipressin 1 expression and decreased as gene/protein expression diminished. We conclude that cells may transiently use increased expression of the DSCR1 (Adapt78) gene product calcipressin 1 to provide short-term protection against acute oxidative stress and other calcium-mediated stresses, whereas chronic overexpression may be associated with Alzheimer disease progression.

Animals↗

Vulnerability-stress factors in development of posttraumatic stress disorder.

Log-linear chi 2 analyses were conducted to examine potential interactions between the presence of precrime axis I psychiatric diagnoses and differential levels of crime stress in association with posttraumatic stress disorder (PTSD) in a community sample of 295 female crime victims. High crime stress was defined as crime that included either perceived life threat, actual injury, or completed rape. Crime stress level was significantly associated with PTSD after the crime. Thirty-five percent of subjects with high crime stress exposure met criteria for PTSD, as opposed to 13% of those with low crime stress exposure. Precrime diagnosis was not associated with high crime stress exposure, indicating that this is not a vulnerability factor for exposure to crime characteristics associated with increased rates of PTSD. There were no significant independent associations between precrime axis I diagnoses and PTSD after the crime. However, a significant interaction was observed among crime stress level, precrime depression, and PTSD such that the rate of PTSD was substantially higher in association with precrime depression only in the high crime stress exposure group. Major findings are consistent with previous results implicating trauma exposure as the primary factor in development of PTSD. However, the results indicate that precrime depression may constitute a vulnerability factor for development of PTSD under conditions of high crime stress exposure.

Adult↗

The effects of daily stress and stressful life events on the clinical symptomatology of patients with lupus erythematosus.

OBJECTIVE: The purpose of this study was to verify whether stress worsens the clinical symptomatology perceived by patients with lupus erythematosus. Toward this end, we considered two types of stressors-daily stress and high-intensity stressful life events. METHODS: In 46 patients with systemic lupus erythematosus and 12 patients with chronic lupus discoid, we studied the stress they experienced daily for 6 months and their disease symptoms. During this period, we also analyzed the levels of C3 and C4 complements and anti-DNAn antibodies. The systemic lupus erythematosus activity (assessed by the Systemic Lupus Activity Measures) and cumulative organ damage (assessed by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) were also analyzed. RESULTS: We did not find that high-intensity stressful life events produced a worsening of the symptomatology of the disease. However, using a time-series analysis (Box-Jenkins), we found that a high percentage of lupus patients (74.1%) perceived a worsening in their clinical symptomatology due to the effects of daily stress. Of this 74.1%, 53.4% worsened the same day they suffered the perceived daily stress, and the remaining 20.7% experienced an increase in symptoms both the same day and the following day. Subsequent Mann-Whitney analyses showed that the patients who worsened for 2 days because of the effects of stress had greater lupus activity, as evaluated by their levels of C3, C4, and anti-DNAn. CONCLUSION: Daily stress, and not stressful life events, worsened the clinical symptomatology perceived by lupus erythematosus patients. This increase extended at times to 2 days, and was associated with greater lupic activity.

Adult↗

Beta-adrenergic responsiveness in stress-sensitive and stress-resistant pigs.

This study investigated whether enhanced metabolic responsiveness to beta-adrenergic stimulation might explain the liability of the stress-sensitive pig to develop an acidosis during stressful situations. Blood lactate, pH, PCO2 and heart rate response to an intravenous infusion of isoprenaline were examined in three lines of pentobarbitone anaesthetized, atropinized pigs. The lines were Pietrain X Hampshire which had been selected over eight generations for a positive reaction to the halothane test (stress-sensitive); Pietrain X Hampshire which had been selected over eight generations for no reaction to the halothane test (stress-resistant) and British Landrace which had been selected over four generations for a positive halothane reaction (stress-sensitive). The metabolic responses to isoprenaline were greater in the stress-sensitive Pietrain X Hampshire line than the stress-resistant line. The stress-sensitive Landrace pigs, however, had smaller changes in pH and PCO2 in response to isoprenaline than the stress-resistant Pietrain X Hampshire pigs. This inconsistent trend across the three lines led to the conclusion that enhanced beta-adrenergic responsiveness was not the likely cause of stress sensitivity.

Animals↗

The reduction of skeletal muscle lesions after experimental stress in stress-susceptible pigs protected with dantrolene.

Malignant hyperthermia (MH) is a naturally occurring disease of stress-susceptible (SS) pigs subjected to triggering agents or stress. MH is characterized by accelerated muscle metabolism and hyperthermia due to abnormally increased myoplasmic Ca2+ levels. Dantrolene is used for the treatment of MH and acts by reducing the myoplasmic Ca2+ levels. Muscle lesions can be induced by experimental restraint stress in SS pigs and are suspected to be caused by increased myoplasmic Ca2+ levels. This experiment was performed in order to study if stress induced muscle lesions could be reduced by dantrolene. Nine SS pigs were exposed to experimental restraint stress provoked by a 12 min intravenous (i.v.) infusion of the depolarizing myorelaxant succinylcholine. Five pigs were orally dosed with dantrolene (5 mg/kg), twice, about 24 and 5 h before the stress (group A). The other four pigs were treated with a single i.v. infusion of dantrolene (5 mg/kg), 30 min before stress (group B). The animals were necropsied approximately 48 h after the stress and 24 skeletal muscles were examined macro- and microscopically. No clinical signs of MH occurred during the experiment. The required dose of succinylcholine was higher in group B (0.08 mg/kg/min) than in group A (0.03 mg/kg/min) indicating decreased sensitivity to succinylcholine in SS pigs after i.v. treatment with dantrolene. The pigs in group A, but not in group B showed slightly increased serum levels of creatine kinase (CK) and aspartate aminotransferase (ASAT) at time of necropsy. A significant reduction in acute muscle lesions was observed in both groups, especially in group B, when compared with SS pigs subjected to restraint stress, but not treated with dantrolene. The muscle lesions induced by the stress model are considered to be induced by increased myoplasmic Ca2+ levels since they can be reduced by dantrolene treatment.

Animals↗

Age-dependent effects of chronic stress on ACTH and corticosterone responses to an acute novel stress.

Aging effects on the hypothalamic-pituitary-adrenocortical system have been studied primarily in the sedentary, environmentally deprived laboratory rat. Since it is known that chronic activation changes the responsiveness of the hypothalamic-pituitary-adrenocortical system, the present experiments were undertaken to determine whether age-related effects on this system would differ between sedentary and chronically stressed rats. Groups of 6- and 20-month-old F-344 rats were exposed to daily sessions of a 2-way shock-escape procedure over a 6-month period. When the rats were 12 (adult) and 26 months of age (old), pituitary-adrenocortical responses to an acute, novel stimulus were examined in young and old chronically stressed and age-matched control rats. Young and old control rats showed essentially the same corticosterone response to an acute motion stress. Chronic stress exposure increased the corticosterone response to the novel acute stressor in young but not in old rats. ACTH levels in response to acute stress were significantly reduced in old control rats compared to young control animals. Chronic stress did not change the ACTH acute stress response in young animals, whereas in old animals chronic stress elevated the ACTH responsiveness so that the old rats showed stress-induced ACTH levels that were comparable to the young animals. In conclusion, the effects of chronic stress on the function of the hypothalamic-pituitary-adrenocortical system are age-dependent, and environmental factors can significantly influence the progression of aging of the hypothalamic-pituitary-adrenal system.

Acute Disease↗

High stress responsivity predicts later blood pressure only in combination with positive family history and high life stress.

High cardiovascular responsivity to stressors has not consistently improved prediction of later blood pressure increases beyond the predictive effects of baseline pressure. Animal models suggest that genetic susceptibility to hypertension and frequent stress exposure are important modulating factors in stress-related hypertension. Thus in 103 men originally tested at age 18 to 22 years and reassessed 10 years later, interactive effects of genetic susceptibility (defined as 1 or more hypertensive parents) with high stress responsivity (defined as top 25% on the basis of blood pressure and cardiac responses during both reaction time and cold pressor tasks) were examined in relation to follow-up systolic and diastolic levels and to change in blood pressure status from normal (diastolic<80 mm Hg) to marginally elevated (diastolic 85 to 95 mm Hg). Men with the combination of high stress response and hypertensive parents demonstrated higher systolic (P<0.05) and diastolic levels (P<0.05) at follow-up, and they showed a 7-fold increase (7.5, 95% confidence intervals 2.3, 24.3; P<0.001) in relative risk of change in blood pressure status versus men with no family history and a 3-fold increase (3.8, confidence intervals 1.5, 9.6; P<0.004) versus less stress-responsive men who also had hypertensive parents. In 65 men who also provided ratings of daily stress, family historyxstress responsivityxdaily stress interactions were significant in predicting follow-up systolic and diastolic levels (P<0.006 and 0.03, respectively), with highest pressure levels seen when high life stress was reported by high stress responders and/or men with hypertensive parents. In conclusion, results suggest that stress responsivity as a long-term predictor is modulated by both genetic and environmental factors.

Adult↗

Total acetylcholine content, and activities of choline acetyltransferase and acetylcholinesterase in brain and duodenum of SART-stressed (repeated cold-stressed) rat.

The cholinergic activities in SART (specific alternation of rhythm in temperature)-stressed (repeated cold-stressed) rats, which are diseased rats with vagotonic-type dysautonomia, were examined with the following results. A decreased content of total acetylcholine (T-ACh) and increased activities of choline acetyltransferase (CAT) and acetylcholinesterase (ACh) in the basal ganglia and an increase in the T-ACh content and decrease in the AChE activity in the duodenum of SART-stressed rats reached the respective plateaus on day 5 of stress, which were maintained thereafter. CAT activity, however, in the hypothalamus was activated most on day 2. These changes in SART-stressed rats were different from those in simple cold-stressed rats. Subdiaphragmatic vagotomy inhibited the appearance of the changes in the duodenum, but not those in the hypothalamus of SART-stressed rats. The sedative analgesic Neurotropin prevented all the changes in SART-stressed rats described above. These results suggest that cholinergic neurons may be activated in both the hypothalamus and basal ganglia of the brain of SART-stressed rats, and the characteristic peripheral changes of the cholinergic system in the duodenum of SART-stressed rats may be under the control of the parasympathetic center.

Acetylcholine↗

Adaptation of cyanobacteria to UV-B stress correlated with oxidative stress and oxidative damage.

Cyanobacteria must cope with the negative effects of ultraviolet B (280-315 nm) (UV-B) stress caused by their obligatory light requirement for photosynthesis. The adaptation of the cyanobacterium Anabaena sp. to moderate UV-B radiation has been observed after 2 weeks of irradiation, as indicated by decreased oxidative stress, decreased damage, recovered photosynthetic efficiency and increased survival. Oxidative stress in the form of UV-B-induced production of reactive oxygen species was measured in vivo with the oxidative stress-sensitive probe 2',7'-dichlorodihydrofluorescein diacetate. Photooxidative damage by UV-B radiation, including lipid peroxidation and DNA strand breakage, was determined by a modified method using thiobarbituric acid reactive substances and fluorometric analysis of DNA unwinding. Photosynthetic quantum yield was determined by pulse amplitude-modulated fluorometry. The results suggest that moderate UV-B radiation results in an evident oxidative stress, enhanced lipid peroxidation, increased DNA strand breaks, elevated chlorophyll bleaching as well as decreased photosynthetic efficiency and survival during the initial exposure. However, DNA strand breaks, photosynthetic parameters and chlorophyll bleaching returned to their unirradiated levels after 4-7 days of irradiation. Oxidative stress and lipid peroxidation appeared to respond later because decreases were observed after 7 days of radiation. The survival curve against irradiation time exhibited a close relationship with the changes in photosynthetic quantum yield and DNA damage, with little mortality after 4 days. Growth inhibition by UV-B radiation was observed during the first 7 days of radiation, whereas normal growth resumed even under UV-B stress thereafter. An efficient defense system was assumed to come into play to repair photosynthetic and DNA damage and induce the de novo synthesis of UV-sensitive proteins and lipids, allowing the organisms to adapt to UV-B stress successfully and survive as well as grow. No induction of mycosporine-like amino acids (MAA) was observed during the adaptation of Anabaena sp. to UV-B stress in our work. The adaptation of the cyanobacterium correlated with and could be caused by the oxidative stress and oxidative damage.

Adaptation, Physiological↗

Effects of angiotensin II on regional brain noradrenaline metabolism in non-stressed and stressed rats.

By measuring levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in various rat brain regions, the effects of angiotensin II (AT II) injected intracerebroventricularly (ICV) were investigated in non-stressed and stressed rats. Immobilization stress with a wire mesh was employed. Immobilization stress induced significant increases in MHPG-SO4 levels in all brain regions examined, i.e., hypothalamus, amygdala, thalamus, midbrain, hippocampus, cerebral cortex and locus coeruleus (LC) region, which suggests that stress increases NA release in these regions. AT II (1 and 10 micrograms), injected ICV 5 min before exposure to stress for 60 min, attenuated stress-induced increases in MHPG-SO4 levels in the hypothalamus, thalamus and amygdala. AT II, injected ICV in non-stressed rats at 65 min before sacrifice, significantly elevated MHPG-SO4 levels in the midbrain, cerebral cortex, thalamus and LC region. These results indicate that the attenuating effect of AT II on stress-induced increases in brain NA release are, in part, related to the reduction of fear and/or anxiety of the animals exposed to stress.

Angiotensin II↗

Responsiveness and habituation of soluble ICAM-1 to acute psychosocial stress in men: determinants and effect of stress-hemoconcentration.

We studied the psychophysiology of soluble intercellular adhesion molecule-1 (sICAM-1) in 25 apparently healthy middle-aged men who underwent an acute psychosocial stressor three times with one week apart. Measures of the biological stress response were obtained at week one and three. The magnitude of the sICAM-1 stress response showed no habituation between individual visits. At week one, cognitive stress appraisal independently predicted integrated sICAM-1 area under the curve (AUC) between rest, immediately post-stress, and 45 min and 105 min post-stress (beta=0.67, p=0.012, deltaR(2)=0.41). Diastolic blood pressure AUC (beta=-0.45, p=0.048, deltaR(2)=0.21) and heart rate AUC (beta=0.44, p=0.055, deltaR(2)=0.21) were independent predictors of sICAM-1 AUC at week three. Adjustment for hemoconcentration yielded a decrease in sICAM-1 levels from rest to post-stress (p<0.001). Stress responsiveness of plasma sICAM-1 was predicted by stress perception and hemodynamic reactivity and affected by stress-hemoconcentration but unrelated to cortisol reactivity and not readily adapting to repeated stress.

Acute Disease↗

[The activity of the monoaminergic systems of the rat hypothalamus in acute stress after chronic stressing].

The influence of chronic stress (footshock combined with randomized light flashes) on acute stress-induced (immobilization) release of noradrenaline, dopamine and serotonin in rat lateral hypothalamus was assessed by microdialysis. The chronic stress resulted in an increase and prolongation of the acute stress-induced release of noradrenaline but not of dopamine and serotonin. The increased rate of accumulation of dioxyphenylacetic acid and unchanged accumulation of homovanillic acid (dopamine metabolites) and dopamine during and after the acute stress in chronically stressed animals reflect a rise of synthetic activity of catecholaminergic systems in response to acute stress and reuptake increase. Marked stress-induced increase in hydroxyindoleacetic acid in chronically stressed rats without any changes in the ST dynamics may be regarded in a similar way. A significant increase in potassium-stimulated release of all the studied monoamines was found while their basal level remained unchanged. The conclusions was made that the hyperergic release of neurotransmitters may be the basis of an inadequate response of animals to acute stress, i.e., one of the neurotic symptoms.

Acute Disease↗

[Application of the thermoelastic stress imaging method to prosthodontics. (2) Basic study of the stress field of artificial molar teeth, in which the existence of saliva was considered].

A basic study was conducted utilizing a thermoelastic stress imaging method for stress analysis of model of simplified artificial molars based on an interocclusal contact relationship. This involved examining the effect of artificial saliva application on a stress field in a situation where occlusal pressure was applied in a dynamic sliding movement. As a result, the following conclusions were obtained. 1. The thermoelastic stress imaging method allowed the stress field to be determined artificial saliva application at distributed load due to plane contact in dynamic sliding movement. 2. Compared with the case of non-saliva application, in a squaremodel having a sliding movement and to which artificial saliva was applied, the pattern of the high compressive stress area was found to be a circle or an ellipsoid. This showed a slight dispersion trend at 10 degrees, with the contact plane as the boundary, and the dispersion of stress concentration began to become clearer at 20; stress concentration on the contact plane tended to disappear at 30 degrees, and sliding was conspicuous and determination impossible at 45 degrees. 3. Results showed that 10 degrees was a transition angle at which a different aspect was shown, representing a trend in a stress field pattern change accompanying an increase in the facet bevel angle when artificial saliva was applied. 4. From the results of stress analysis using the square-shape sliding movement model to which artificial saliva was applied, 10 degrees to 20 degrees of facet bevel of artificial molars was considered preferable in consideration of the presence of saliva.

Bite Force↗

Stress, anticipatory stress, and psychologic measures related to sleep bruxism.

This study examined (1) the relationships between electromyographic-measured nocturnal bruxism, self-reported stress, and several personality variables, and (2) the relationship between belief in a stress-bruxism relationship and self-reported stress. One hundred adult bruxers completed a battery of personality questionnaires, indicated whether they believed in a stress-bruxism relationship, presented for a dental examination, and had dental impressions taken. Subsequently, electromyographic measurements of bruxing frequency and duration were recorded for fifteen consecutive nights. Prior to each night's measurements, subjects indicated their levels of stress for the immediately preceding 24 hours. No overall relationship was established between electromyographic measures and the personality variables nor between electromyographic measures and self-reported stress. Correlations between electromyographic measures and self-reported stress were statistically significant for eight individual subjects. Further, subjects with high levels of stress reported more anxiety, irritability, and depression, and less denial. Subjects who believed in a stress-bruxism relationship reported greater stress.

Adolescent↗