Chest pain with normal coronary arteries.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
BACKGROUND/AIM: Severe stress results in a catabolic state with nitrogen (N) loss via hepatic urea synthesis, and in most situations a sensation of pain. Our purpose was to establish whether pain per se upregulates liver function as to urea synthesis. METHODS: Ten healthy male volunteers were investigated on 3 occasions in a crossover design. Self-controlled electrical pain was applied to the abdominal skin for 30 min to an intensity of 8 on a visual analogue scale from 0 to 10. Next, the electric profile was reproduced during local analgesia (mepivacaine 2.5 mg/kg bw), and the pain was scored to only 0.5. Finally, there was a control experiment with no intervention. Alanine infusion (1 mmol/kg/h) was started 2 h before intervention and continued throughout the investigation. Urea-N synthesis rate (UNSR) was estimated hourly as urinary excretion corrected for accumulation in body water and gut hydrolysis. RESULTS: Pain increased the Functional Hepatic Nitrogen Clearance (FHNC) assessed by the ratio UNSR/AAN (in the 3 h following pain) by 20% (22.7+/-1.2 vs 19.0+/-0.7 l/h (control), p<0.05). FHNC during local analgesia was in between (21.1+/-1.1 l/h) but not significantly different from either of the two other experiments. Mean blood amino-N concentration (AAN) and mean UNSR were comparable in the three situations. There was no difference in serum glucagon among experiments, but pain increased serum cortisol (452+/-15 vs 233+/-20 nmol/l (control), p<0.001) and plasma adrenaline (104+/-16 vs 58+/-9 pg/ml (control), p<0.05). CONCLUSION: Acute, severe atraumatic pain induces an increase in the ability of the liver to convert amino- to urea-N, and thus acts as a catabolic stimulus via regulation of liver function. The measurements of known endocrine regulators of urea synthesis do not explain the phenomenon. The present data, however, suggest the hypothesis that the effects of pain were attenuated by local analgesia. If this is confirmed by further experiments, it would indicate a signal transmission to the liver which has not been previously described.
OBJECTIVES: The authors present the clinic results obtained with the bulbourethral sling application with pubic bone anchorage (Invance) in patients with stress urinary incontinence. MATERIAL AND METHODS: From July to December 2003, 10 slings were implanted in men between the 60's and the 83 years old (average 72.6 years), whose incontinence appeared after prostatic surgery (retro pubic radical prostatectomy, perineal radical prostatectomy, radical cystoprostatectomy with Camey II neobladder, transurethral resection, transvesical prostate adenomectomy). RESULTS: After 9 months follow-up (3 to 7 months), 8 patients (80%) are continent (without need of using any pad) and 2 (20%) show minimum leakage with effort (need of 1 to 2 daily pads). All are satisfied with the surgery result. Two patients referred perineal pain, which was solved with Paracetamol. There was no case of perineal haematoma, infection, rejection or urethral erosion. CONCLUSION: The bulbourethral sling with bone anchorage is a rather invasive procedure, of easy technical execution, with high continence rates and associated to low morbidity. Although the presented results been an incentive to the technique prolongation, it would be necessary a higher tracking: and higher global experience in order that this sling affirm and transform itself in an alternative to the artificial sphincter in selected cases.
To examine the specific effects of cutaneous pain on electroencephalographic (EEG) activities, tonic painful and non-painful sensations in left forearm were induced by intradermal injection of capsaicin 100 microg/20microl and the same volume of vehicle, respectively, in 15 healthy males. The EEG data acquired in five experimental conditions: (i) baseline A; (ii) non-painful vehicle injection; (iii) baseline B; (iv) painful capsaicin injection and (v) waning pain, were analyzed and compared with analysis of variance. Only the painful capsaicin injection evoked significant decreases of theta, alpha-1 and alpha-2 powers over the centro-parieto-occipital regions compared with baseline B. No significant difference in EEG activation between the non-painful vehicle injection and painful capsaicin injection was found. This implicates that the observed topographic EEG activation is not specific for pain but probably related to the cutaneous stimulation.
Suspensions of autologous, washed platelets were intracutaneously injected at the volar forearms of healthy volunteers. Injections of serum and vehicle served as control. Subjects and experimenter were blind with respect to the sequence of injections. In contrast to serum and solvent solution, platelets induced graded burning pain lasting several minutes. Platelet but not serum or vehicle injections dose-dependently caused large axon-reflex flares. At the site of platelet injections an induration developed and in parallel delayed mechanical and heat hyperalgesia was observed. Hyperalgesia to pressure and impact stimulation reached a maximum after 6 h and subsided during the following 48 h. Also, the threshold to heat stimuli decreased moderately by about 1 degree C, on average, after 24 h. Neither indurations nor hyperalgesia could be detected at the injection sites of serum or vehicle. The pathophysiological significance of this new inflammatory model for the research of posttraumatic hyperalgesia is discussed.
The hypothesis of reorganization of the primary somatosensory cortex in states of chronic pain was assessed in 10 low back pain patients and nine matched healthy controls. Intracutaneous electric stimuli were applied to the left back and index finger at a standard, a non-painful and a painful intensity. Magnetic fields were recorded by a 37-channel BTi biomagnetometer from the hemisphere contralateral to the site of stimulation. The power of the early evoked magnetic field (< 100 ms) elicited by painful stimulation of the painful back in very chronic patients was elevated relative to that elicited by painful back stimulation of healthy controls and showed a linear increase with chronicity (r = 0.74). The maximum activity elicited in primary somatosensory cortex was shifted more medially in the very chronic back pain subjects. These data suggest that chronic pain is accompanied by cortical reorganization and may serve an important function in the persistence of the pain experience.
This study examined the effects of intravenous administration of sodium amytal (SA), a medium action barbiturate, on cutaneous limb temperatures and sympathetic skin responses (SSR) to electrical stimulation. Eight normal volunteers and 13 patients with musculoskeletal pain, somatoform pain disorders or nerve/root injury (with findings strictly limited to the distribution of the distribution of the involved nerve) were compared to 15 patients with Complex Regional Pain syndromes (one of whom had documented nerve injury). The Complex Regional Pain Syndromes (CRPS) patients were characterized by the presence of severe diffuse limb pain and extraterritorial sensory, sudomotor and vasomotor abnormalities (i.e., not confined to the site of injury or the distribution of the injured nerve). The CRPS patients were different from the normal controls and the non-CRPS patients in their tendency to warm significantly many of their limbs (not just the symptomatic ones). SSR were reduced or lost in a few limbs only in all three groups, irrespective of the increase or decrease of limb temperature and the side of symptoms. We argue that the enhanced thermogenic effect of SA in CRPS patients is due to generalized central changes of thermoregulatory control specifically in this group.
Whether the pathogenesis of cluster headache (CH) is peripheral or central is still matter of debate. An involvement of central structures related to pain perception and modulation, which also causes an alteration of the physiological pattern of pain perception in CH, has been hypothesized. We investigated the pattern of brain response to pain in normal subjects and CH patients by evaluating the cerebral blood flow (CBF) changes using an experimental model of tonic aching pain stimulation, the cold water pressor test (CWPT). CBF was assessed quantitatively by the Xe-133 inhalation method and single photon emission tomography (SPET), at rest and during CWPT, as previously described (Di Piero et al., 1994). CWPT was performed in 12 volunteers and in seven patients with CH. All the CH patients had a left-sided headache and were studied in a headache-free phase out of the cluster period. During CWPT, volunteers showed a significant CBF increase in the contralateral primary sensorimotor (P < 0.001), frontal (P < 0.01) and temporal (P < 0.002) regions and thalamus (P < 0.01) and in the ipsilateral temporal (P < 0.005) and anterior cingulate (P < 0.01) regions. During left-hand stimulation (ipsilateral to the headache side) by CWPT in CH patients, CBF changes were significantly lower than those observed in volunteers in the contralateral primary sensorimotor region (P < 0.0005) and thalamus region (P < 0.01). There were no significant differences in the brain response observed during the stimulation of the hand contralateral to the headache side. In conclusion, in a headache-free phase out of the cluster period, the pattern of cerebral activation during tonic pain stimulation of the hand ipsilateral to the headache side is critically modified in CH patients in areas which are probably involved in the detection of the stimulus intensity. This modification may reflect a marker of a biological modification of the pain conveyance system. The fact that it is also present out of the active period of the disease, suggests a possible involvement of central tonic pain mechanisms in the pathogenesis of CH.
Previous functional imaging studies have demonstrated a number of discrete brain structures that increase activity with noxious stimulation. Of the commonly identified central structures, only the anterior cingulate cortex shows a consistent response during the experience of pain. The insula and thalamus demonstrate reasonable consistency while all other regions, including the lentiform nucleus, somatosensory cortex and prefrontal cortex, are active in no more than half the current studies. The reason for such discrepancy is likely to be due in part to methodological variability and in part to individual variability. One aspect of the methodology which is likely to contribute is the stimulus intensity. Studies vary considerably regarding the intensity of the noxious and non-noxious stimuli delivered. This is likely to produce varying activation of central structures coding for the intensity, affective and cognitive components of pain. Using twelve healthy volunteers and positron emission tomography (PET), the regional cerebral blood flow (rCBF) responses to four intensities of stimulation were recorded. The stimulation was delivered by a CO2 laser and was described subjectively as either warm (not painful), pain threshold just painful), mildly painful or moderately painful. The following group subtractions were made to examine the changing cerebral responses as the stimulus intensity increased: (1) just painful - warm; (2) mild pain - warm; and (3) moderate pain - warm. In addition, rCBF changes were correlated with the subjective stimulus ratings. The results for comparison '1' indicated activity in the contralateral prefrontal (area 10/46/44), bilateral inferior parietal (area 40) and ipsilateral premotor cortices (area 6), possibly reflecting initial orientation and plans for movement. The latter comparisons and correlation analysis indicated a wide range of active regions including bilateral prefrontal, inferior parietal and premotor cortices and thalamic responses, contralateral hippocampus, insula and primary somatosensory cortex and ipsilateral perigenual cingulate cortex (area 24) and medial frontal cortex (area 32). Decreased rCBF was observed in the amygdala region. These responses were interpreted with respect to their contribution to the multidimensional aspects of pain including fear avoidance, affect, sensation and motivation or motor initiation. It is suggested that future studies examine the precise roles of each particular region during the central processing of pain.
Although the interaction between sleep and pain is generating considerable interest (NIH Technology Assessment Panel, 1996), it is still unknown if chronic pain is the cause or effect of poor sleep. To further this understanding, subjects free of pain and sleep problems need to be studied in order to assess their response to pain during sleep, defined as a behavioral and a physiological state in which sensory processing is altered. (For example, while auditory perception remains active, other sensory inputs are facilitated, attenuated, or suppressed (Velluti, 199746 degrees C) was statistically greater in the lighter sleep stage 2 (48.3%) than in the deeper stages 3&4 (27.9%). A nocifensive behavioral-motor response was associated with only 2.5% of the 351 heat pain stimuli. Two other markers of sleep quality-sleep stage shift and awakening-were not influenced by the thermal stimuli. None of the subjects demonstrated any burns in the morning following the thermal stimulations applied during sleep. We conclude that the processing of nociceptive inputs is attenuated across sleep stages.
In Fabry disease, an X-linked alpha-galactosidase A deficiency, painful crises and limb paresthesias are possibly linked to thermal exposure. Small nerve fiber function has not yet been tested after cold challenge. In two Fabry patients (15 and 17 years old), their heterozygote mother, their healthy sister, and eight controls, we determined warm and cold perception thresholds at the dorsal foot and the lower medial calf (method of limits, Somedic-Thermotest), before and 1, 5, 10 and 15 min after 30 s immersion of one leg into 5 degrees C water. Discomfort was rated from 0 to 10. At baseline, thermal thresholds of all participants were normal. In contrast to controls, the patients tolerated 30 s cold stimulation only with interruptions. The mother aborted stimulation after 6 s because of pain. The patients and their mother reported intense burning pain and numbness during and after stimulation. After cold exposure, thermal sensation was highly abnormal for 20 min in one and 80 min in the other brother. In controls, thermal thresholds were somewhat elevated after stimulation but normalized within 10.0+/-4.6 min. Discomfort during cold exposure was rated 8-10 by the patients and their mother, but 3-5 by the healthy persons. We assume that glycolipid accumulation in cutaneous and vasa nervorum vessels as well as small nerve axons accounts for skin and small fiber malperfusion during cold induced vasoconstriction. Transitory ischemia initiated burning pain and prolonged small fiber dysfunction.
INTRODUCTION: Mucosal melanomas are rare tumors, and primary sinonasal malignant melanomas uncommon tumors that are frequently misclassified. Differential diagnosis should rule out other sinonasal malignancies, including carcinoma, lymphoma, sarcoma, and olfactory neuroblastoma. CASE: We report two new cases of sinonasal melanoma. One involved a 68-year-old man being followed for chronic sinusitis, despite antibiotics; he presented a tumor of the right nasal cavity. The second case was that of a 77-year-old woman, referred for painful gingival swelling shown to involve osteolytic growth in the left maxillary sinus. In both cases, pathologic examination of the biopsy samples concluded that these were sinonasal malignant melanomas. DISCUSSION: Histologically, the diagnosis is very difficult because of the polymorphic features of this tumor, and immunohistochemical studies are very important. The relative inaccessibility of the mucosa to self-examination often delays diagnosis and leads to late detection and poor prognosis.
There is international agreement that dyspepsia refers to pain or discomfort centered in the upper abdomen. However, the term 'discomfort' has been variably defined. While other symptoms may often be simultaneously present, gastro-oesophageal reflux disease can usually be clearly distinguished by the presence of predominant heartburn. Dyspepsia is a frequent reason for consultation in primary care and in gastrointestinal practice. With the widespread availability and utilization of endoscopy, it has become evident that a structural (or organic) explanation is found in only a minority of patients presenting with dyspepsia. Operationally, functional dyspepsia is defined as persistent or recurrent dyspepsia for 3 or more months in the absence of a clinically identifiable structural disease causing the symptoms. It has been proposed, based on symptoms, that functional dyspepsia be subdivided into symptom subgroups to promote patient homogeneity. The initially proposed 'clustering' of symptoms into ulcer-like and dysmotility-like functional dyspepsia has proved a dismal failure because of the considerable overlap observed, the lack of stability over time and the failure to identify robust pathophysiological abnormalities or responses to therapy. A subcategorization based upon the most bothersome symptom is theoretically more attractive but needs to be prospectively and rigorously tested.
OBJECTIVE: To assess the central EMG inhibitory action of tendon afferent input in muscle diseases. METHODS: The EMG inhibition elicited by electrical stimulation over muscle tendons was tested in 13 healthy voluntary subjects and 8 patients who had a primary muscle disease with a mild force deficit. Electrical stimuli were delivered to the tendon of the extensor carpi radialis muscle at the wrist during tonic voluntary isometric contraction at 50% of the maximum EMG level. The EMG signal was recorded by surface electrodes over the extensor carpi radialis muscle. RESULTS: The prestimulus background EMG level was reduced in 7 out 8 of the patients. Both groups had the same phases of EMG modulation following tendon stimulation (TE1, TI1, TE2) and their latency and amplitude did not differ significantly. Conversely, the area of TI1 was significantly larger (i.e. the inhibition decreased) in patients ([mean+/-SD] absolute area: controls=4.1+/-1.6 mVms, patients=6.9+/-2.9 mVms, P<0.05). CONCLUSIONS: In muscle dysfunction there are serial 'upstream' changes of central inhibitory systems, probably to maximize the residual muscle power of the affected muscle.
OBJECTIVE: To evaluate the effects of spinal immobilization on healthy participants. METHODS: A systematic review of randomized, controlled trials of spinal immobilization on healthy participants. RESULTS: Seventeen randomized, controlled trials compared different types of immobilization devices, including collars, backboards, splints, and body strapping. For immobilization efficacy, collars, spine boards, vacuum splints, and abdominal/torso strapping provided a significant reduction in spinal movement. Adverse effects of spinal immobilization included a significant increase in respiratory effort, skin ischemia, pain, and discomfort. CONCLUSIONS: Data from this review provide the best available evidence to support the well-recognized efficacy and potential adverse effects of spinal immobilization. However, comparisons of different immobilization strategies on trauma victims must be considered in order to establish an evidence base for this practice.
Early, middle and late latency somatosensory evoked potentials (SEPs) elicited by cutaneous electrical stimulation (painful vs. non-painful) of right and left hands were recorded. The aims were to study (1) if lifelong use of dominant right hand would result in different SEP topographies compared to non-dominant left hand stimulation, (2) if painful and non-painful stimuli resulted in different SEP activation patterns for the different latency components and (3) if these results were consistent between two areas of the hand. Electrical stimuli were applied cutaneously above the thenar and hypothenar muscles of the left and right hand. A two-way repeated measures ANOVA was used to test the effects of laterality and intensity for a given peak amplitude and latency. Statistical results yielded no significant difference in peak amplitude for either thenar and hypothenar between the two hands. In contrast, a significant difference in amplitude was observed for 6 components for each stimulus location when the two intensities were compared. These components were found at early, middle and late latencies. No significant latency shift was observed between the two hands. Only the P30 component showed a significant latency shift for both locations with the painful condition having the shorter latency. Thus, life-long use of the dominant hand does not generate detectable changes in cortical evoked activity to sensory input from the skin above thenar and hypothenar muscles. Several SEP components across the time course (0-400 ms) showed increased amplitude when the stimulus was increased from non-painful to painful intensity.
A 51-year-old woman was referred for pain in the right temporomandibular joint (TMJ) and the trismus. Conventional radiography showed a radiopaque area in the disk, which suggested calcification. At surgery, multiple, round-to-ovoid cartilagenous nodules were found in the joint cavity. Synovectomy and diskectomy were carried out via a pre-auricular incision to remove the nodules. Examination under light microscopy confirmed the diagnosis of synovial osteochondromatosis (SOC). The disk contained a large ossified mass. To our knowledge, this is the first reported example of SOC accompanied by ossification of a large part of the disk.
Endothelial nitric oxide synthase (eNOS) has been implicated in various brain and peripheral pathologies such as renal failure, heart failure or stroke. Consequently, the mortality rate of aged eNOS knockout mice (eNOS-/-) was higher than that of age-matched (18-22 months old) controls. Only seven of the original 14 eNOS-/- animals that participated in the study reached the age of 18 months or older, whereas no control mice died during this life span. In order to assess the behavioral and neurochemical consequences of chronic eNOS deficiency we examined whether the surviving aged eNOS-/- mice showed changes in terms of motor, emotional, exploratory and neurochemical parameters. Aged eNOS-/- mice showed reduced exploratory activity in the open-field with no habituation observable neither within sessions nor after repeated exposures. Pole test performance of eNOS-/- mice was comparable to controls. In the elevated plus-maze eNOS-/- mice did not differ from controls in terms of time spent in and entries into arms, but showed less locomotion on the open arms. The most prominent neurochemical alterations in the forebrains of aged eNOS-/- mice were: (a) increased acetylcholine levels in the neostriatum; (b) decreased noradrenaline concentrations in the ventral striatum; and (c) lower serotonin levels in the frontal cortex and ventral striatum. The present findings suggest that mice which survived chronic eNOS-deficiency into old age, show some behavioral and neurochemical phenotypes distinct from adult eNOS-/- mice.