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

Identifying the cause of recurrent chest pain may be difficult. Significant coronary artery disease must be excluded before patients can be assured that their symptoms are truly "noncardiac." A normal coronary angiogram is the most definitive test but this may not preclude the presence of a new "fly in the ointment," i.e., microvascular angina. Musculoskeletal pain syndromes, psychological problems, and esophageal disorders, including both esophageal motility disorders and gastroesophageal reflux disease, are the most common causes of noncardiac chest pain. Nearly 30% of these patients will have an esophageal motility disorder, although its clinical relevance in the asymptomatic patient is controversial. Simple, inexpensive, provocation tests (most commonly edrophonium, bethanechol, and/or balloon distention) have been developed to recreate motility-related chest pain in the laboratory. These tests can identify the esophagus as the source of pain, but in most cases they do not direct therapy. Other disadvantages of provocation tests include the lack of a gold standard reference point, side effects, and the need for placebo because of a subjective end point. Recently, ambulatory esophageal pH and pressure monitoring have been used to define precisely the cause of esophageal chest pain. These systems can record multiple episodes of pain for up to 24 hours in an outpatient setting and have shown that gastroesophageal reflux (rather than motility disorders) is the most common esophageal cause of pain. However, these studies also suggest that many episodes of chest pain do not have an identifiable esophageal cause. Furthermore, this equipment is expensive, uncomfortable, may alter normal activity, and is not useful in patients having infrequent pain episodes. Psychological disturbances should be carefully sought in any patient with noncardiac chest pain: Many patients have anxiety, depression, or panic attacks that may complicate or contribute to their reported symptoms. It is questionable if these patients need additional testing. Rather, the challenge of the future is to prove that the multitude of tests aid in the overall treatment and outcome of patients with noncardiac chest pain.
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PMID:Overview of diagnostic testing for chest pain of unknown origin. 159 63

Recurring substernal chest pain is an important clinical problem, causing anxiety for patients and their physicians because of the fear of possible cardiac disease. The differential diagnosis includes coronary artery disease, oesophageal disorders such as acid reflux disease and motility disturbances, musculoskeletal problems, psychological disorders including panic attacks, and a new 'fly in the ointment'--microvascular angina. History alone usually cannot distinguish cardiac from non-cardiac chest pain. After exclusion of significant coronary artery disease, attention must be turned to oesophageal disorders, which may be seen in as many as 50% of these patients. Oesophageal motility disorders, particularly the nutcracker oesophagus, are common, but the relationship between pain and abnormal contraction pressures is not well established. Provocative tests such as edrophonium (Tensilon) and balloon distension help to identify the oesophagus as the source of chest pain but do not direct therapy. Recent studies with ambulatory oesophageal monitoring suggest that gastro-oesophageal reflux may be a more common cause of chest pain than motility disorders. This is an important finding as acid reflux is a treatable problem, while therapies for motility disorders may only worsen reflux disease. The recent observation that oesophageal disorders are frequently associated and interact with psychological disorders such as anxiety, depression, somatization and panic attacks complicates the evaluation and understanding of chest pain. How these various abnormalities may be linked is an unresolved issue. Increased central nervous system stimulation and altered visceral and/or central pain sensitivity could be the common factors. It is hoped that further research into these areas will lead to new understandings of and possible solutions to the complex problem of non-cardiac chest pain.
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PMID:Investigation and management of non-cardiac chest pain. 191 53

All in all, panic disorder with or without agoraphobia is a very satisfying illness to treat. Most patients enter treatment with considerable pain and disability and within a few weeks to months are free of panic attacks, no longer fearful of them, and no longer phobic. Panic disorder must be distinguished from generalized anxiety, and signs of agoraphobia must be sought during the initial diagnosis. Drug therapy is effective for panic disorder, while agoraphobia may respond to drug therapy or to a range of cognitive therapies.
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PMID:Solving panic disorder problems. When your patients' fears thwart their lives. 197 3

Presentation of an observation of alarming thoracic pain, during a panic attack. Actualization of this psycho-somatic pathology concerning the epidemiologic, etiopathogenic and therapeutic aspects as well as its cardiovascular repercussion.
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PMID:[Alarming chest pains in the young adult. Apropos of a case]. 204 37

Because panic disorder has an underlying biologic and probably genetic basis, the role of factors outside the organism in initiating and sustaining panic is often overlooked. The authors review certain exogenous factors that seem capable of triggering attacks and/or increasing their frequency and intensity: self-administered pharmacologic agents (caffeine, alcohol, nicotine, over-the-counter cold preparations, cannabis, cocaine); habits (sleep deprivation, diet, exercise, relaxation, hyperventilation); and aspects of the environment (fluorescent lighting, life stressors). There may be a specificity to the action of some of these factors, because certain factors previously thought to trigger panic attacks (e.g., pain, hypoglycemia) have been proved not to have this effect. Although the clinical significance of many of the exogenous factors discussed still awaits empirical confirmation, attention to such factors during the initial evaluation of a patient with panic disorder may be helpful in formulating a successful treatment plan.
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PMID:Exogenous factors in panic disorder: clinical and research implications. 327 68

The above results with intracerebral drug injection and electrical brain stimulation in rats indicate that enhancement of GABAergic activity in the dorsal CG or in the MH raises the threshold of electrical stimulation inducing aversive behavior when applied to these brain areas. Conversely, drug-induced reduction of GABA action in the dorsal CG or in the MH leads to aversive-like behavioral changes. Therefore, GABAergic fibers seem to exert tonic inhibition on neuronal groups in the CG and MH integrating aversive behavioral states. Anxiolytics may cause anti-aversive effects by enhancing this GABAergic modulation. As discussed elsewhere, serotonergic and opioid mechanisms are also likely to operate in periventricular brain areas. In conjunction with GABAergic mechanisms, they may be involved in the pathophysiology of anxiety, panic attacks and pain, as well as in the therapeutic action of anxiolytics, anti-panic drugs and centrally-acting analgesics.
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PMID:Role of GABA in the anti-aversive action of anxiolytics. 376 23

Thalamic structures involved in the unpleasant emotional or affective aspect of pain are poorly understood. We now describe studies of the region of the thalamic principal somatosensory nucleus (Vc) performed before thalamotomy for tremor in a patient who also had panic disorder. Microstimulation in the region posterior to Vc evoked chest pain, including a strong affective dimension, almost identical to that occurring during his panic attacks, as measured using a questionnaire. Results in our other patients indicate that stimulation-associated pain with a strong affective dimension occurred only in those patients who had previously experienced spontaneous pain with a strong affective component. These results are consistent with stimulation-evoked activation of limbic structures, which are connected through cortex with the region posterior to Vc and involved in the affective dimension of pain through conditioning by previous experience.
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PMID:Stimulation in the human somatosensory thalamus can reproduce both the affective and sensory dimensions of previously experienced pain. 758 11

Noncardiac chest pain is a common but important clinical challenge with respect to diagnostic strategy as well as therapeutic intervention. The most common esophageal disorder associated with chest pain syndrome is gastroesophageal reflux; 24-hour ambulatory monitoring of esophageal pH and the determination of the symptom index are useful in patient evaluation. A high frequency of abnormal esophageal motility has been reported in noncardiac chest pain, but its clinical significance remains controversial. Patients with chest pain and normal coronary angiogram may have microvascular angina. Musculoskeletal conditions account for at least 10% of the cases of noncardiac chest pain. The potential effects of stress and altered psychological states in this phenomenon must be considered. The role of panic attacks in the production of pain needs to be clarified. Investigations to elucidate the exact cause of chest pain as well as its treatment should be individualized to the patient.
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PMID:Pathophysiology and management of noncardiac chest pain. 760 35

Physiological dependence on benzodiazepines is accompanied by a withdrawal syndrome which is typically characterized by sleep disturbance, irritability, increased tension and anxiety, panic attacks, hand tremor, sweating, difficulty in concentration, dry wretching and nausea, some weight loss, palpitations, headache, muscular pain and stiffness and a host of perceptual changes. Instances are also reported within the high-dosage category of more serious developments such as seizures and psychotic reactions. Withdrawal from normal dosage benzodiazepine treatment can result in a number of symptomatic patterns. The most common is a short-lived "rebound" anxiety and insomnia, coming on within 1-4 days of discontinuation, depending on the half-life of the particular drug. The second pattern is the full-blown withdrawal syndrome, usually lasting 10-14 days; finally, a third pattern may represent the return of anxiety symptoms which then persist until some form of treatment is instituted. Physiological dependence on benzodiazepines can occur following prolonged treatment with therapeutic doses, but it is not clear what proportion of patients are likely to experience a withdrawal syndrome. It is also unknown to what extent the risk of physiological dependence is dependent upon a minimum duration of exposure or dosage of these drugs. Withdrawal phenomena appear to be more severe following withdrawal from high doses or short-acting benzodiazepines. Dependence on alcohol or other sedatives may increase the risk of benzodiazepine dependence, but it has proved difficult to demonstrate unequivocally differences in the relative abuse potential of individual benzodiazepines.
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PMID:The benzodiazepine withdrawal syndrome. 784 56

The brain cholecystokinin-B/gastrin receptor (CCK-B/gastrin) has been implicated in mediating anxiety, panic attacks, satiety, and the perception of pain. The canine and human CCK-B/gastrin receptors share 90% amino-acid identity and have similar agonist affinities. These receptors can be selectively blocked by the non-peptide benzodiazepine-based antagonists L365260 (ref. 8) and L364718 (ref. 9); however, the binding of these antagonists to the human and canine receptors differs by up to 20-fold, resulting in a reversal of affinity rank order. Here we report the identification of a single amino acid in the sixth transmembrane domain of the CCK-B/gastrin receptor that corresponds to valine 319 in the human homologue and which is critical in determining the binding affinity for these non-peptide antagonists. We show that it is the variability in the aliphatic side chain of the amino acid in position 319 that confers antagonist specificity. Substitution of valine 319 with a leucine residue decreases the affinity for L365260 20-fold while concomitantly increasing the affinity for L364718. An isoleucine in the same position of the human receptor selectively increases affinity for L364718. Interspecies differences in the aliphatic amino acid occupying this single position selectively affect antagonist affinities without altering the agonist binding profile. We therefore conclude that the residues underlying non-peptide antagonist affinity must differ from those that confer agonist specificity. To our knowledge, these findings are the first example in which a critical antagonist binding determinant for a seven-transmembrane-domain peptide hormone receptor has been identified.
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PMID:A single amino acid of the cholecystokinin-B/gastrin receptor determines specificity for non-peptide antagonists. 845 20


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