Objective Evaluation of Chronic Low-Back Pain Using Serum Lipids: The Role of the Doctor-Patient Relationship.

Statistical data show that pain intensity in patients with low back pain is associated with a higher BMI, total serum cholesterol, and triacylglycerol levels. The objective of our study was to evaluate how these associations are dependent on the nature of the patient-doctor relationship. Eighty-nine patients hospitalized with chronic low-back pain (50 women, 39 men; average age: 64.5 ± 12.7 years) were assessed over a 3-year period. A serum lipid analysis was conducted (LDL-C, HDL-C, and total cholesterols) at admission in parallel with a subjective evaluation of pain intensity, which was assessed using a numeric rating scale. The participating physician assigned, based on their personal interaction with the patient, an attribute of affinity (positive, neutral, and negative) towards them. Current serum lipid levels and pain intensity were correlated relative to these attributes. Pain intensity did not differ between the groups assigned positive or negative attributes of affinity. In patients belonging to the "positive" group, pain intensity correlated positively with total cholesterol (p=0.01) and LDL cholesterol (p=0.007). No correlations were found in the "negative" group or when the patient-doctor relationship was ignored. We found a significant association between subjectively assessed low back pain intensity and serum levels of total and LDL cholesterol in patients with whom the physician had a positive affinity. A positive affinity with the patients having chronic pain and the patient's trust in their physicians may ultimately mean that the patient's statement about pain is more credible, which may retroactively affect the outcome of therapy.

The sight of one's own body: Could qEEG help predict the treatment response in anorexia nervosa?

Aims of the study: The study aims to identify the differences in brain activity between participants with anorexia nervosa and healthy control using visual stimulus conditions combined with the quantitative dense-array EEG recording analysis method called Brain Activation Sequences (BAS). Materials and methods: 23 participants with anorexia nervosa and 21 healthy controls were presented with visual stimuli, including the subject's facial expressions and body images. The 128-channel EEG data were processed using BAS and displayed as activity in up to 66 brain regions. Subsequent cluster analysis was used to identify groups of participants exhibiting area-specific activation patterns. Results: Cluster analysis identified three distinct groups: one including all healthy controls (HC) and two consisting of all participants with anorexia (AN-I with 19 participants and AN-II with four participants). The AN-I and AN-II groups differed in their response to treatment. Comparisons of HC vs. AN confirmed the dominance of the right cerebral hemisphere in participants with anorexia nervosa in two of the three reported conditions. The facial expressions condition, specifically the facial reaction expressing disgust, indicates the existence of a social attentional bias toward faces, whereas emotions remained undetected in participants. High limbic activity, medial frontal gyrus involvement, low fusiform cortex activity, and milder visual cortex activity in healthy controls compared to participants indicate that the facial expression stimulus is perceived by healthy subjects primarily as an emotion, not as the face itself. In the body image condition, participants showed higher activity in the fusiform gyrus and right insula, indicating activation of the brain's "fear network." Conclusion: The study describes a specific pattern of brain activation in response to facial expression of disgust and body images that likely contributes to social-cognitive and behavioral impairments in anorexia. In addition, the substantial difference in the pattern of brain activation within the participants with AN and its association with treatment resistance deserves special attention because of its potential to develop a clinically useful prediction tool and identify potential targets for, for example, neuromodulatory treatments and/or individualized psychotherapy.

Effects of Transcranial Direct Current Stimulation Treatment for Anorexia Nervosa.

Background: Anorexia nervosa (AN) is a life-threatening illness with poor treatment outcomes. Although transcranial direct current stimulation (tDCS) is a promising non-invasive brain stimulation method, its effect in patients with AN remains unclear. Objective: This study investigated changes in maladaptive eating behavior, body mass index (BMI), and depression after 10 sessions of anodal tDCS over the left dorsolateral prefrontal cortex (DLPFC). Methods: In this double-blind, randomized controlled trial, 43 inpatients with AN were divided to receive either active (n = 22) or sham (n = 21) tDCS over the left DLPFC (anode F3/cathode Fp2, 2 mA for 30 min). All patients filled the Eating Disorder Examination Questionnaire (EDE-Q) and Zung Self-Rating Depression Scale (ZUNG), and their BMI was measured. These values were obtained repeatedly in four stages: (1) before tDCS treatment, (2) after tDCS treatment, (3) in the follow-up after 2 weeks, and (4) in the follow-up after 4 weeks. Results: Primary outcomes (EDE-Q) based on the ANOVA results do not show any between-group differences either after the active part of the study or in the follow-up. Secondary analysis reveals a reduction in some items of EDE-Q. Compared with sham tDCS, active tDCS significantly improved self-evaluation based on body shape (p < 0.05) and significantly decreased the need of excessive control over calorie intake (p < 0.05) in the 4-week follow-up. However, the results do not survive multiple comparison correction. In both sham and active groups, the BMI values improved, albeit not significantly. Conclusion: We did not observe a significant effect of tDCS over the left DLPFC on complex psychopathology and weight recovery in patients with AN. tDCS reduced the need to follow specific dietary rules and improved body image evaluation in patients with AN. Tests with a larger sample and different positions of electrodes are needed. Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT03273205.

Changes of BMI, steroid metabolome and psychopathology in patients with anorexia nervosa during hospitalization.

Anorexia nervosa (AN) is associated with various alterations including the dysfunction of the HPA axis and consequently the hypercortisolemia and deficit in sex hormones but the comprehensive evaluation of changes in circulating steroids during the hospitalization of AN patients is lacking. We investigated the effect of realimentation of women with AN during hospitalization on 45 circulating steroids, the relationships between BMI, its change during hospitalization and physical activity, on one side and initial levels and their changes for two adipokines, circulating steroids, anorexia-specific (hunger, appetite and satiety), and anorexia non-specific symptoms (anxiety, depression fatigue, sleep, and body pain) on the other side. We included 33 women with anorexia who were hospitalized for 38(35, 44) days (median with quartiles). The increase of BMI from the initial value 15.2 (13.2, 16.6) kg/m2 was 1.69 (1.37, 2.66) kg/m2. The patients with more severe anorexia showed higher activity in 7ß-, and 16α-hydroxylation of androgen precursors, which declined during hospitalization. Otherwise, the 7α-hydroxylation activity is higher in AN patients with less severe malnutrition and the ratio of 5-androstene-3ß,7α,17ß-triol to 5-androstene-3ß,7ß,17ß-triol increased during the realimentation. Our data allow to speculate that the intensive 7ß-, and 16α- and possibly also the 7α-hydroxylation of C19 Δ5 steroids participate in the pathophysiology of anorexia by additional catabolism of substrates available for synthesis of active androgens and estrogens. However, the question remains whether the synthetic analogues of 7α/ß- and 16α-hydroxy-steroids prevent the catabolism of the sex steroid precursors, or further activate the "energy wasting" mitochondrial thermogenic metabolism.

Dissatisfaction with own body makes patients with eating disorders more sensitive to pain.

Body image represents a multidimensional concept including body image evaluation and perception of body appearance. Disturbances of body image perception are considered to be one of the central aspects of anorexia nervosa and bulimia nervosa. There is growing evidence that body image distortion can be associated with changes in pain perception. The aim of our study was to examine the associations between body image perception, body dissatisfaction, and nociception in women with eating disorders and age-matched healthy control women. We measured body dissatisfaction and pain sensitivity in 61 patients with Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition diagnoses of eating disorders (31 anorexia nervosa and 30 bulimia nervosa) and in 30 healthy women. Thermal pain threshold latencies were evaluated using an analgesia meter and body image perception and body dissatisfaction were assessed using Anamorphic Micro software (digital pictures of their own body distorted into larger-body and thinner-body images). Patients with eating disorders overestimated their body size in comparison with healthy controls, but the two groups did not differ in body dissatisfaction. In anorexia and bulimia patient groups, body dissatisfaction (calculated in pixels as desired size/true image size) correlated with pain threshold latencies (r=0.55, p=0.001), while between body image perception (determined as estimation size/true image size) and pain threshold, no correlation was found. Thus, we demonstrated that in patients with eating disorders, pain perception is significantly associated with emotional contrary to sensory (visual) processing of one's own body image. The more the patients desired to be thin, the more pain-sensitive they were. Our findings based on some shared mechanisms of body dissatisfaction and pain perception support the significance of negative emotions specific for eating disorders and contribute to better understanding of the psychosomatic characteristics of this spectrum of illnesses.

Can Anxiety Tested in the Elevated Plus-maze Be Related to Nociception Sensitivity in Adult Male Rats?

Methamphetamine (MA) is one of the most addictive psychostimulant drugs with a high potential for abuse. Our previous studies demonstrated that MA administered to pregnant rats increases pain sensitivity and anxiety in their adult offspring and makes them more sensitive to acute administration of the same drug in adulthood. Because individuals can differ considerably in terms of behaviour and physiology, such as rats that do not belong in some characteristics (e.g. anxiety) to average, can be described as low-responders or high-responders, are then more or less sensitive to pain. Therefore, prenatally MA-exposed adult male rats treated in adulthood with a single dose of MA (1 mg/ml/kg) or saline (1 ml/kg) were tested in the present study. We examined the effect of acute MA treatment on: (1) the anxiety in the Elevated plus-maze (EPM) test and memory in EPM re-test; (2) nociception sensitivity in the Plantar test; (3) the correlation between the anxiety, memory and the nociception. Our results demonstrate that: (1) MA has an anxiogenic effect on animals prenatally exposed to the same drug in the EPM; (2) all the differences induced by acute MA treatment disappeared within the time of 48 hours; (3) there was no effect of MA on nociception per se, but MA induced higher anxiety in individuals less sensitive to pain than in animals more sensitive to pain. In conclusion, the present study demonstrates unique data showing association between anxiety and nociceptive sensitivity of prenatally MA-exposed rats that is induced by acute drug administration.

Common mechanisms of pain and depression: are antidepressants also analgesics?

Neither pain, nor depression exist as independent phenomena per se, they are highly subjective inner states, formed by our brain and built on the bases of our experiences, cognition and emotions. Chronic pain is associated with changes in brain physiology and anatomy. It has been suggested that the neuronal activity underlying subjective perception of chronic pain may be divergent from the activity associated with acute pain. We will discuss the possible common pathophysiological mechanism of chronic pain and depression with respect to the default mode network of the brain, neuroplasticity and the effect of antidepressants on these two pathological conditions. The default mode network of the brain has an important role in the representation of introspective mental activities and therefore can be considered as a nodal point, common for both chronic pain and depression. Neuroplasticity which involves molecular, cellular and synaptic processes modifying connectivity between neurons and neuronal circuits can also be affected by pathological states such as chronic pain or depression. We suppose that pathogenesis of depression and chronic pain shares common negative neuroplastic changes in the central nervous system (CNS). The positive impact of antidepressants would result in a reduction of these pathological cellular/molecular processes and in the amelioration of symptoms, but it may also increase survival times and quality of life of patients with chronic cancer pain.

Role of dehydroepiandrosterone and cortisol in nociceptive sensitivity to thermal pain in anorexia nervosa and healthy women.

OBJECTIVES: Anorexia nervosa (AN) patients represent a natural model of relationship between changed hormonal level and pain perception due to lower level of sex hormones and consistently described increased pain threshold. As the adrenal stress steroid hormones (cortisol and DHEA) are known to be also changed in AN (and share a common precursor), our study was aimed to analyze the association between these hormones and pain perception in AN patients and control healthy women. METHODS: The pain threshold latencies to radiant heat stimuli were measured in 20 DSM-IV diagnosed patients with AN and in 21 healthy women. Blood samples were collected in the morning hours and analyses of the plasma levels of dehydroepiandrosterone (DHEA), its conjugated sulfate ester (DHEA-S) and cortisol were implemented. RESULTS: Thermal pain threshold was higher in AN than in healthy women and correlated negatively with the level of DHEA and positively with cortisol/DHEA(S) ratio. No significant correlation between thermal pain and hormones was found in healthy women. If both groups were pooled together, the rest pain threshold correlated negatively with DHEA-S (r=-0.42, p=0.008). CONCLUSION: We showed for the first time that sensitivity to thermal pain in women is dependent on DHEA-S and on cortisol/DHEA(S) ratio in patients with AN.

Assessment of chronic benign and cancer pain using blood plasma biomarkers.

OBJECTIVE: The objective was a systematic study of the biochemical markers which are descriptive for the dynamics of pain processes. MATERIALS AND METHODS: The patients who had not been systematically treated for pain prior to their participation in this study consisted of 20 non-oncological (mean age 56.5 years) and 20 oncological patients (mean age 64.8 years). Pain intensity, assessed using the visual analogue scale (VAS) on a scale from 0-10, and the following biochemical parameters were measured during the initial patient workups: blood serum total protein, glucose, total cholesterol, HDL cholesterol, LDL cholesterol, atherosclerotic indexes, triacylglyceroles, apolipoprotein A, apolipoprotein B, albumin, alpha1 globulin, alpha2 globulin, beta globulin and gamma globulin. Biochemical measurements were repeated as soon as VAS assessments fell below 5. Therapy in non-oncological patients involved administration of NSA and weak opioids; while oncological patients received NSA, medium strength and strong opioids, and antidepressants. RESULTS: Prior to therapy, concentration of albumin in serum, HDL cholesterol, and apolipoprotein A were lower, whereas CRP and alpha1 globulin were higher in oncological patients compared to non-oncological patients. After therapy, levels of glucose and alpha1 globulin were significantly higher and levels of apolipoprotein A were lower in oncological patients compared to non-oncological patients. Irrespective of diagnosis, patients treated with antidepressants showed higher levels of gamma globulin compared to non treated patients. CONCLUSIONS: We can conclude that observed biochemical markers in patients with malignancies are more similar to the values of patients with chronic benign pain than to the values of patients with acute pain.

Two patients with eating disorders treated by naltrexone.

According to a recent literature review on the opioid mechanism in eating disorders, we found that there is increasing reason to re-examine the treatment potential of naltrexone. The endogenous opioid system belongs to the important modulators of food intake. The eating disorders share many traits with substance dependence models. We present two case histories of time-limited naltrexone therapy to show that, in clinical practice, individualized indication may contribute to short-term improvement and to prediction of a different long-term treatment outcome.

The effect of laparotomy on hydroxyl radicals, singlet oxygen and antioxidants measured by EPR method in the tails of rats.

OBJECTIVES: The aim of the study was to demonstrate that direct measurement of hydroxyl radicals and singlet oxygen in the tail of living rats is possible. The basic level of hydroxyl radicals and singlet oxygen were measured and the effects of antioxidants on their levels were studied in the tail of living anaesthetized rats after acute postoperative pain. Laparotomy was performed as the source of acute abdominal pain. After closure of the abdominal cavity, the animals began to awaken within 30-60 minutes. They were left to recover for 2-3 hours; then they were reanesthetized and the effect of antioxidants was measured on the numbers of hydroxyl radicals and singlet oxygen via blood in the tail. METHODS: The laparotomy was preformed under general anesthesia (Xylazin and Ketamin) using Wistar rats. After recovery and several hours of consciousness they were reanaesthetized and free radicals and singlet oxygen were measured. An antioxidant mixture (vitamins A, C, D and Selenium) was administered intramuscularly prior to the laparotomy. All measurements were done on the tail of anaesthetized animals. In this particular article, the effect of antioxidants is only reported for hydroxyl radicals. RESULTS: After laparotomy, which represented both somatic and visceral pain, hydroxyl radicals and singlet oxygen were increased. Antioxidant application prior to laparotomy decreased the numbers of hydroxyl radicals. CONCLUSION: Results are in agreement with our previous finding regarding the increase in hydroxyl free radicals and singlet oxygen following nociceptive stimulation, in this case a combination of both somatic and visceral pain. The administered antioxidants mitigated the increase. This is further confirmation that direct measurement of free radicals and singlet oxygen represents a very useful method for the biochemical evaluation of pain and nociception.

Modulation of thermal pain perception by stress and sweet taste in women with bulimia nervosa.

OBJECTIVES: To investigate if the increased pain threshold in women with bulimia nervosa (BN) may be due to chronic stress-induced analgesia. METHODS: We measured thermal pain threshold latency, blood pressure and heart rate in 21 women with BN and 21 healthy women (HW) under six consecutive conditions: rest I, mental arithmetic task, rest II, eating sweet food, rest III, cold-pressor test. RESULTS: Thermal pain threshold latency was longer in BN than in HW in all six conditions. It increased during mental arithmetic test and remained increased during the rest of the experiment in both groups. In the BN group, the increase of pain threshold during mental arithmetic was positively correlated with illness duration. The differential modulation of pain threshold by stress in BN and HW could not be explained by autonomic system reactivity. In HW, the pain threshold increased more during eating and blood pressure increased more during mental stress; in BN, the pain threshold was highest in the mental stress condition and blood pressure was most increased during eating. During the cold pressor test, women with BN showed smaller blood pressure increase and tolerated the cold for shorter time than HW. CONCLUSION: The observed marked modulation of pain threshold by experimental stress suggests that stress-induced analgesia is unlikely to account for baseline pain insensitivity in BN. Increased pain threshold in BN is a stable yet incompletely understood phenomenon, which may be related to the predisposition to or maintenance of the disorder.

Assessment of biochemical markers in patients with pain of vascular origin.

The aim of this study was to analyse blood plasma biochemical parameters in patients with pain of vascular origin. Blood samples were taken from 62 patients (38-86 years of age) with critical limb ischaemia, claudication or lower limb embolism, and from a control group. The samples were taken at the time of hospital admission, 1 h after surgery, 24 h after surgery, and before discharge. Pain intensity was assessed as mild, moderate or intense. The following biochemical parameters were measured: C reactive protein, total protein, albumin, total cholesterol, HDL and LDL cholesterol, glucose, triglycerides, reduced glutathione, malondialdehyde (MDA), and total antioxidative capacity. In the control subjects, MDA increased postoperatively, whereas albumin, total protein, HDL and total cholesterol decreased. In patients with claudication triglycerides and LDL cholesterol also decreased postoperatively. In patients with critical limb ischaemia, reduced glutathione and antioxidative capacity decreased postoperatively and MDA increased. Except in patients with embolism, MDA and C reactive protein increased following surgery. Patients with critical limb ischaemia and embolism reported the worst preoperative pain. In patients with ischaemia, intense pain persisted during the whole postoperative period while in patients with embolism pain continuously decreased. At different time intervals, pain intensity was related to different biochemical markers. We suggest that the described blood plasma changes might play an important role in pain assessment and pain management.

Normalizing effect of bright light therapy on temperature circadian rhythm in patients with eating disorders.

OBJECTIVES: Light and food are important synchronizers of circadian rhythmicity. In eating disorders, the circadian rhythms of food intake and temperature are abnormal. METHODS: We analyzed the effect of the morning light application on the circadian rhythm of tympanic temperature and its association with hunger and mood changes in the sample of 25 female patients hospitalized with DSM-IV diagnosis of eating disorders (14 bulimia nervosa and 11 anorexia nervosa) and in 6 healthy women. RESULTS: Light therapy reduced interindividual variability of the temperature acrophase, synchronized the temperature and hunger rhythms and showed an antidepressant effect on patients with eating disorders. Bright light therapy normalized the circadian rhythm of body temperature in both anorexic and bulimic patients: phase advanced rhythm was delayed and phase delayed rhythm was advanced. In contrast with anorexic patients, the majority of bulimic patients had normal temperature rhythm before the therapy and this rhythm was not changed by the therapy. CONCLUSION: The light therapy normalized temperature circadian rhythm in patient with eating disorders. We hypothesize that the light therapy can also contribute to improvement of pathological eating pattern because of the functional connections between light and food entrained oscillators. The light may help to restore the irregular circadian rhythmicity induced by chaotic food intake.

Motor cortex stimulation in rats with chronic constriction injury.

Motor cortex stimulation (MCS) has gained a significant role in treatment of neuropathic pain. In order to evaluate effect of MCS in experimental animals we applied MCS to rats with neuropathic pain, which was evoked by chronic constriction injury (CCI) to the left sciatic nerve. Pain thresholds of both hind limbs were measured before, immediately after MCS, 1 h after MCS and 1 day after MCS. Effect of the stimulation was studied with respect to laterality (contralateral and ipsilateral MCS) and duration (short-term 10-min and long-term 1-h stimulation). It was found out that in control rats MCS did not affect thermal nociceptive thresholds. However, in CCI animals following results were obtained: difference score (difference in paw withdrawal latency between ligated and non-ligated hind limb) significantly decreased after both short- and long-term contralateral MCS; the difference score after the long-term ipsilateral MCS (related to the ligated hind limb) was not significantly different from that of intact animals; the effects of the contralateral short-term and the ipsilateral long-term stimulation faded within 1 h after the end of MCS, while the effect of the contralateral long-term MCS remained 1 h after the end of the MCS and faded within 24 h. It is concluded that MCS in experimental animals exerts similar effects as in human suffering from neuropathic pain and that the effect might be evoked from both cerebral cortices.

Different transfer of nociceptive sensitivity from rats with postnatal hippocampal lesions to control rats.

Hippocampal lesions in newborn rats alter the development of mechanisms involved in the processing of nociception. The hippocampal lesion was induced by the bilateral infusion, into the lateral cerebral ventricles, of 0.25 microL of saline containing either 0.25 micromol quinolinic acid (QUIN) and/or 0.25 micromol N-acetyl-L-aspartyl-L-glutamate (NAAG) on postnatal day 12. The same amount of sterile saline was injected into the sham-operated animals (group SHAM). It was expected that the QUIN- and NAAG-lesioned rats would exhibit some differences in thermal pain perception; however, we wanted to know if the control rats would exhibit, at least in part, similar changes in pain perception as their chemically lesioned siblings with which they were housed. Young adult NAAG-injured rats exhibited increased withdrawal latencies in the tail-flick and plantar tests, whereas young adult QUIN-injured animals exhibited only marginally decreased latencies. Nociceptive responses in the SHAM rats paralleled the littermates that had been neonatally treated with QUIN or NAAG, i.e. the responses in the SHAM(QUIN) group decreased, whereas the responses in the SHAM(NAAG) group increased. No significant changes in nociception were observed in intact animals, regardless of which group they were housed with. Our results show that social factors, which were originally demonstrated only for the pain behavior, may also influence basal nociceptive sensitivity in rats. We concluded that the "sham operation" may have had a long-term, nonspecific impact on nociceptive behavior by inducing behavioral mimicry of other animals.

The effect of motor cortex stimulation in deafferentated rats.

OBJECTIVES: The aim of the study was to describe the effect of motor cortex stimulation (MCS) on pain thresholds in deafferentated rats. SETTINGS AND DESIGN: The effect of MCS was studied in 18 deafferentated and 14 intact laboratory rats, using a standardised plantar test and tail-flick latencies. Two inoxious stimulation electrodes were implanted subdurally over the cerebral cortex and a C5-Th1 dorsal root rhizotomy was performed on the left side. Pain thresholds were measured before and after cortical stimulation. The data were analysed with ANOVA for repeated measures. RESULTS: MCS in intact animals evoked no changes in pain thresholds except for the contralateral forelimb, in which the pain threshold increased after MCS. Following deafferentation, pain thresholds increased in both plantar test and tail-flick in comparison to baseline values. When MCS was applied to the deafferentated animals, the pain thresholds returned to baseline levels. The effect of MCS disappeared within 24 hours. MAIN FINDINGS: 1. MCS in intact animals evoked hypoesthesia in the corresponding contralateral forelimb; 2. deafferentation itself increased pain thresholds in the unaffected limbs; 3. under MCS, pain thresholds in deafferentated rats were not different from pre-dafferentation values; 4. the effect of MCS disappeared in 24 hours and oscillated. CONCLUSIONS: Our results show a similar effect of the stimulation in man and experimental animals despite the differences in the organisation of the cerebral cortex. The use of laboratory animals is promising for further studies in the field of involved antalgic mechanisms of MCS.

Blood serum changes in patients with pain during bone fractures and acute pancreatitis.

OBJECTIVES: Our aim was to evaluate whether some biochemical parameters in the blood serum can establish and discriminate pain intensity of different etiology. METHODS: Three groups of patients hospitalised at the Department of Surgery have been investigated: 1) the patients without pain but with the indicated surgical treatment, 2) the patients with acute pancreatitis, which represents severe pain of the visceral type, and 3) the patients with fractures of upper or lower extremities, which represented acute somatic pain. Whole serum proteins, albumin, C-reactive protein, glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol, triacylglyceroles (triglycerides), apolipoprotein-B and electrophoretic levels of alpha-lipoprotein, beta-lipoprotein and pre-beta-lipoprotein were analysed immediately after the first clinical inspection in the hospital and then 30 days after treatment. RESULTS: The intensity of pain estimated by the visual analogue scale (VAS) was higher in patients with acute pancreatitis than in patients with fractures. In both diagnoses during persisting pain, the products of lipid metabolism such as triacylglyceroles and HDL-cholesterol were enhanced together with glucose levels. Electrophoretic measurements, revealed higher levels of beta-lipoproteins in fractures, and increased values of pre-beta-lipoproteins and alpha-lipoproteins in both groups of patients suffering from pain. After 30 days of treatment some indicators decreased, but when compared with normal values, they were still higher, especially in patients with pancreatitis (HDL-cholesterol, triacylglyceroles, pre-beta-lipoprotein). In control patients without pain symptoms, an increase of LDL cholesterol, triacylglyceroles and beta-lipoprotein were observed during their stay in hospital, which may be considered to be due to hospitalisation stress per se. Acute stress generally influences glucose levels so that their increase cannot be considered as a specific marker of pain intensity. CONCLUSIONS: It may be concluded from our investigation, that the biochemical composition of the blood serum is changing during painful states, although the question still remains open to what extent these changes reflect the pain intensity and to what extent they may modulate the perception of pain.

Free radicals after painful stimulation are influenced by antioxidants and analgesics.

OBJECTIVES: To study the balance between the pro-oxidative and antioxidative defence system after repeated painful stimulation in rats and the efficacy of the administration of different antioxidants (vitamins C, E, A, and selenium), analgesics (acetylsalicylic acid, morphine), and their combinations. METHODS: Mechanical clamping of both hind limbs was applied for 10 min for 5 consecutive days in adult male Wistar rats. The tail-flick latency was measured before and after a 5-day nociceptive stimulation with or without the substance application. The reactive oxygen species (ROS) were determined in the sensorimotor cortex. RESULTS: Painful stimulation increased lipoperoxidation which persisted for up to 15 days after it had been discontinued. A simultaneous injection of antioxidants decreased the levels of TBARS, SOD and GSHPx; however, antioxidants applied one week prior to the painful stimulation were ineffective. A simultaneous injection of analgesics reduced stress-induced analgesia caused by the nociceptive stimulation, but did not affect lipoperoxidation. CONCLUSIONS: A combination of antioxidants with analgesics normalized both the oxidative stress and functional (the tail-flick latency) indicators. These results suggest that the administration of antioxidants in pain treatment may be employed to decrease the doses of analgesics and to prevent the negative impact of reactive oxygen species on nociception.