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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-eight patients previously investigated for suspected angina but shown to have normal coronary arteriograms were reviewed. The prognosis for like expectancy was excellent but 76% were still symptomatic after average follow up of three years. 41% of those re-evaluated were still thought to be describing cardiac-like pain. Full re-investigation showed coronary artery spasm or other causes of myocardial ischemia to be rare whereas oesophageal spasm was a common cause of the pain.
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PMID:Diagnosis and prognosis of chest pain with normal coronary arteriograms. 694 51

Oesophageal spasm may mimic the pain of myocardial ischaemia. Forty-two patients who were thought to have angina until investigations failed to show any cardiovascular abnormality, were examined for oesophageal disease. Ergometrine provocation during oesophageal manometry caused significant deterioration in oesophageal motility, associated with familiar pain, in 24 patients. Ten age-matched controls were examined in a similar way and ergometrine produced motility changes in four and pain in two. Six volunteers with coronary artery stenosis and exercise-induced angina did not develop oesophageal motility changes during the pain. Ergometrine provocation is useful in establishing the diagnosis of oesophageal spasm in patients with recurrent angina-like pain but no cardiac abnormality.
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PMID:Diagnosis of oesophageal spasm by ergometrine provocation. 706 41

The effect of pentagastrin on oesophageal motility was studied in six subjects with idiopathic diffuse oesophageal spasm (IDOS). Pentagastrin was administered by continuous intravenous infusion in doses of 1 microgram/kg/h, 5 micrograms/kg/h, and 10 micrograms/kg/h. Saline infusion was used as a control. No subject experienced pain during pentagastrin infusion. Two developed dysphagia and repetitive contractions with 'wet' swallows during the saline infusion and the lowest pentagastrin infusion. Contraction amplitude was increased only with 'dry' swallows during the 10 micrograms/kg/h infusion period. Contraction duration was increased with both 'wet' and 'dry' swallows during the 1 microgram/kg/h infusions, and with 'dry' swallows during the 10 micrograms/kg/h infusion. Propagation velocity was not altered by pentagastrin. We conclude that gastrin released physiologically by eating probably does not contribute to symptom production in IDOS. Moreover, it seems unlikely that pentagastrin, at least in these doses, can be exploited for diagnostic purposes.
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PMID:Pentagastrin in diffuse oesophageal spasm. 722 56

In this report we show that coronary arterial and esophageal spasm are sometimes clinically indistinguishable. Pain patterns can be identical, nitroglycerin can bring relief, interval electrocardiograms and exercise electrocardiograms generally disclose no abnormalities, coronary arteriograms may be within normal limits or nearly so, and, importantly, an ergonovine provocative test can provoke esophageal spasm accompanied by pain mistaken for Prinzmetal's angina. Accordingly, chest pain in response to the administration of ergonovine is not evidence of coronary arterial spasm without simultaneous arteriographic proof together with changes in the monitoring electrocardiogram. Conversely, gastroenterologists should not expose patients to the risk of ergonovine without prior assurance that the coronary arterial response is normal. Our observations illustrate these points and identify a patient with symptomatic esophageal spasm previously diagnosed as Prinzmetal's angina.
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PMID:Coronary arterial spasm versus esophageal spasm. Response to ergonovine. 723 95

At present, an esophageal origin can be identified in as many as 50% of patients with non cardiac chest pain. In about 1/3 of these patients, gastroesophageal reflux can be documented. In the remaining 2/3 of patients, various disorders of esophageal motility have been described. Abnormal esophageal motility may be classified as nutcracker esophagus, diffuse esophageal spasm, achalasia, hypertensive lower esophageal sphincter, and nonspecific esophageal motility disorders. Simultaneous recording of intraesophageal pH, pressure, and symptoms (combined 24-h pH-metry and manometry) makes it possible to test the temporal association between pain, reflux, or abnormal motility. This review describes the diagnostic evaluation and therapeutic options in patients with non cardiac chest pain. Identification of the esophageal origin of chest pain should improve the therapeutic results.
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PMID:[Esophageal thoracic pain: what can be done?]. 815

Esophageal diseases frequently cause symptoms such as heartburn, epigastric pain and dysphagia. This article discusses the indications, techniques and limitations of currently available diagnostic procedures. Investigation of symptoms should proceed in a logical stepwise manner, beginning with endoscopy to exclude esophagitis or neoplasia. Symptoms due to acid reflux can be identified by 24h esophageal pH-metry to document a temporal association between symptoms and episodes of esophageal acidification. Stationary or ambulatory manometric recording of esophageal pressures can be used to diagnose esophageal motor disorders such as achalasia, nutcracker esophagus, diffuse esophageal spasm, or dysfunction of the upper or lower esophageal sphincter. Combined 24 h pH-manometry should be used to test the temporal association between pain, reflux, or abnormal motility in patients with non-cardiac chest pain. Video-fluoroscopy is the most appropriate technique to diagnose swallowing disorders. Pulmonary aspiration of gastro-esophageal reflux can be documented with scintigraphy.
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PMID:[Motility disorders and assessment methods of the esophagus]. 821 Oct 52

Spastic disorders of the esophagus are found in up to 50% of patients referred for manometry, therapy representing the most prevalent motility disorders in clinical practice. They share in common their manifestations of hypermotility, one of two principal types of esophageal motor dysfunction. Diffuse esophageal spasm is segregated from the nonspecific spastic disorders because of its demonstrated interference with bolus transit. However, the overlap among the spastic disorders in manifestation, course, and management is great; segregation of any disorder within this group is not of paramount importance. Spastic disorders, pain reproduction with provocative testing, and psychological abnormalities are coprevalent in patients with unexplained symptoms, but a cause-effect relationship of the motor abnormalities with the other findings is not established. The physician's charge in determining the relevance of a spastic disorder to the clinical presentation and for creating a treatment plan is to establish a direct relationship of motor dysfunction with symptoms-a task that may require correlation of transit abnormalities with symptoms using tests other than manometry. A variety of treatment options, invasive and noninvasive, are available today for patients who have spastic disorders, and each is effective in appropriately selected candidates.
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PMID:Spastic disorders of the esophagus. 919 29

We report the case of a 61-year-old-man with an eosinophilic esophagitis with esophageal motor disorder associated with toxocariasis. He complained of non cardiac chest pain and had eosinophilia leading to the detection of Toxocara canis infection. Pain persisted despite treatment of toxocariasis. Basal manometry was normal but ambulatory 24-hour manometry-pHmetry showed diffuse esophageal spasm. Ultrasonography showed a thickening of the esophageal musculature in the two inferior thirds of the esophagus. After failure of treatment with sodium cromoglycate steroids and esophageal dilatation, calcium antagonists were partially effective. A long esophageal myotomy was performed permiting the disappearance of symptoms. The histological examination of a side myotomy biopsy showed an eosinophilic infiltration of the esophageal muscle layer. This observation leads to discuss the possible relation between toxocariasis, the esophageal motor disorder and the eosinophilic infiltration of the esophageal muscle layer.
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PMID:[Myotomy for esophageal muscular hypertrophy with eosinophil infiltration of the esophagus associated with toxocariasis revealed by esophageal motor disorder]. 976 93

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

Subtypes of functional dyspepsia (FD), including refluxlike dyspepsia, ulcerlike dyspepsia, dysmotility-like dyspepsia, and nonspecific dyspepsia, have been described and are widely used clinically. However, these symptom patterns often overlap, and the terms are insufficient for indicating all FD symptoms. In this study, we divided 71 FD patients into two groups: patients with or without pain. Group I, the pain dyspepsia group, included patients in whom the main symptoms were epigastralgia and/or chest pain. Group II, the painless dyspepsia group, included patients without pain, in whom the symptoms were nausea, vomiting, and heartburn. We examined the relationship between esophageal function and psychiatric factors in the test groups and compared them with a control group. Of the FD patients, 19.7% [8 (25%) of 32 group I patients, 6 (15.4%) of 39 group II patients] had esophageal motility disorders, such as nutcracker esophagus and diffuse esophageal spasm. The LES pressure of group I was higher than that of group II by esophageal manometry (P < 0.05). In 17 (53.1%) of 32 group I patients and 31 (79.5%) of 39 group II patients, psychiatric disorders (38.0% had depressive disorder and 21.1% had an anxiety disorder) were diagnosed following DSM III-R criteria. Group II tended to be more depressive than group I (P = 0.0508). Psychological assessment scores, STAI-I and STAI-II, were higher in groups I and II than in the control group (P < 0.001). Long-term distress, anxiety, and depression seem to influence the symptoms of FD patients. Esophageal dysmotility may be an important functional abnormality of FD.
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PMID:Esophageal motility and psychiatric factors in functional dyspepsia patients with or without pain. 1054 63


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