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

Esophageal pain is transmitted via the sympathetic nervous system to the spinal cord, in which pain from visceral and somatic sources ascends to higher centers in the brain. Primary afferent neurons are bipolar, with the peripheral end specialized to be a sensory receptor. Nociceptors of somatosensory afferents are free nerve endings that can be activated by mechanical, thermal, or chemical stimuli. Esophageal nociceptive neurons have not been specifically identified but probably are also free nerve endings. Most esophageal spinal mechanoreceptors have been shown to be nociceptive. Some esophageal mechanonociceptors have a wide dynamic range and respond to physiologic and painful stimuli, while others have a high threshold of stimulation and are solely nociceptive. Esophageal spinal afferents have their cell bodies in the dorsal root ganglia and contain substance P and calcitonin gene-related peptide. These putative neurotransmitters are transported in both the peripheral and central directions of bipolar afferent neurons. Primary afferent neurons are likely to also contain an excitatory amino acid neurotransmitter such as glutamate. Centrally, nociceptive primary afferents terminate on neurons in specific layers of the dorsal horn of the spinal cord. Convergence of multiple visceral afferents with somatic afferents onto the same dorsal horn neurons may explain referred pain. A patient's inability to distinguish esophageal from cardiac pain may be due to convergence of pain pathways. Second-order neurons in the dorsal horn project in the anterolateral system to the brain. Within the anterolateral system, nociception ascends in the spinothalamic, spinoreticular, and spinomesencephalic tracts. The thalamus relays fast pain to the postcentral areas of the parietal lobe of the cortex. Pathways to the reticular formation are slow and may mediate the increased arousal that occurs in response to pain. The spinomesencephalic tract projects to midbrain sites including the periaqueductal gray. Organ-specific pathways in the brain have yet to be defined, but neuroanatomic tracing techniques employing neurotropic viruses are being developed. The perception of pain can be influenced at multiple levels, such as the receptor in the esophagus, the synapses in the dorsal horn of the spinal cord or thalamus, or the cortex. A fundamental mechanism of modulating nociception is descending inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanisms of esophageal pain. 159 55

Pain site and radiation and the effect of various foods were studied prospectively in a consecutive series of patients with chronic upper abdominal pain. Patients followed for less than one year were excluded unless peptic ulcer or abdominal malignancy had been diagnosed or laparotomy had been carried out. A total of 632 patients were eligible for the first study and 431 for the second. Gastric ulcer pain was more likely to be left hypochondrial (17%) compared with pain from duodenal ulcer (4%) or from all other conditions (5%). It was less likely to be epigastric (54%) compared with duodenal ulcer pain (75%). Oesophageal pain was more likely to be both retrosternal and epigastric (25%) compared with non-oesophageal pain (2%). Radiation to the back was more common in peptic ulcer (31%) and biliary pain (35%) compared with functional pain (20%). Pain precipitation by fatty foods was commoner in biliary disease (40%) than in duodenal ulcer (11%), peptic ulcer (9%), or non-ulcer dyspepsia (19%). Orange, alcohol, and coffee precipitated pain more frequently in duodenal ulcer (41%, 50%, and 43% respectively) than in biliary disease (17%, 0%, and 14% respectively). Chilli precipitated pain in one quarter to one half of subjects regardless of diagnosis. Approximately one tenth of all subjects avoided chilli, curry, coffee, and tea because of medical or other advice.
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PMID:Chronic upper abdominal pain: site and radiation in various structural and functional disorders and the effect of various foods. 162 52

Esophageal pain was investigated in 200 consecutive patients prior to surgical correction of reflux. the pain has been analyzed to determine its characteristic and its atypical features. Arm distribution of pain and exercise induced pain were the most a typical features and led to diagnostic difficulty. Although acid perfusion studies reproduced some component of the pain in 94% of patients, reproduction of arm pain was possible in only 37.2% of those with this symptom. The importance of cardiologic evaluation in patients with atypical esophageal pain is emphasized.
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PMID:Characteristics of esophageal pain. 694 44

Visceral pain in infants represents a complexity of interacting neural, developmental, psychosocial, and environmental factors, which must be separately and conjointly evaluated. Inhibitory mechanisms are not fully developed in infants and thus nociception is not readily dampened. Heightened behavioral responses to pain (e.g., crying) are likewise not easily inhibited. Esophageal pain and behaviors perceived by the caregiver to represent pain (e.g., crying and retching) can potentially affect normal growth and development. The response of the infant to pain and other visceral sensory stimuli and the ability to cope with these sensations (painful and nonpainful) are shaped by the relationship of the infant with the primary caregiver, usually the mother. Neural mechanisms of pain transmission and inhibition are reviewed, as well as biopsychosocial and environmental characteristics that can shape or contribute to infant pain syndromes. Proposed multifaceted clinical treatment strategies are aimed at decreasing efforts to dampen excitatory neural sensory signaling and improving the mother/infant relationship and maternal behavioral response to the crying infant.
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PMID:Visceral pain in infants. 798 68

Hypersensitivity is a common finding in visceral disorders. Therefore, in the development and testing of analgesics for the treatment of visceral pain, it is important to establish an experimental pain model of visceral hypersensitivity. Such a model will mimic the clinical situation to a higher degree than pain models where the receptors and peripheral afferents are briefly activated as with, for example, electrical, thermal, and mechanical stimulations. In this study, a model to evoke experimental hyperalgesia of the oesophagus with a combination of acid and capsaicin was introduced. The study was a randomised, double-blind, cross-over study. Fifteen healthy volunteers were included. Sensory assessments to mechanical, heat, and electrical stimulations were done in the distal oesophagus, before and after perfusion with a 200 ml solution of acid+capsaicin (180 ml HCL 0.1 M and 2 mg capsaicin in 20 ml solvent) or saline. Oesophageal pain assessment and referred pain areas were evaluated. There were reproducible pain assessments between repetitions within the same day and between days (all P > 0.05). Acid+capsaicin perfusion induced 56% reduction of the pain threshold to heat (P = 0.04), 19% reduction of the pain threshold to electrical stimuli (P < 0.001), 78% increase of the referred pain areas to mechanical stimulation (P < 0.001) and 52% increase of the referred pain areas to electrical stimulus (P = 0.045). All volunteers were sensitised to one or more modalities by acid+capsaicin. The model was able to evoke consistent hyperalgesia and may be useful in future pharmacological studies.
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PMID:Evoked human oesophageal hyperalgesia: a potential tool for analgesic evaluation? 1942 57

Oesophageal pain is one of the most common reasons for physician consultation and/or seeking medication. It is most often caused by acid reflux from the stomach, but can also result from contractions of the oesophageal muscle. Different forms of pain are evoked by oesophageal acid, including heartburn and non-cardiac chest pain, but the basic mechanisms and pathways by which these are generated remain to be elucidated. Both vagal and spinal afferent pathways are implicated by basic research. The sensitivity of afferent fibres within these pathways may become altered after acid-induced inflammation and damage, but the severity of symptoms in humans does not necessarily correlate with the degree of inflammation. Gastro-oesophageal reflux disease (GORD) is caused by transient relaxations of the lower oesophageal sphincter, which are triggered by activation of gastric vagal mechanoreceptors. Vagal afferents are therefore an emerging therapeutic target for GORD. Pain in the absence of excess acid reflux remains a major challenge for treatment.
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PMID:Roles of gastro-oesophageal afferents in the mechanisms and symptoms of reflux disease. 1965 9

Noxious stimuli in the esophagus cause pain that is referred to the anterior chest wall because of convergence of visceral and somatic afferents within the spinal cord. We sought to characterize the neurophysiological responses of these convergent spinal pain pathways in humans by studying 12 healthy subjects over three visits (V1, V2, and V3). Esophageal pain thresholds (Eso-PT) were assessed by electrical stimulation and anterior chest wall pain thresholds (ACW-PT) by use of a contact heat thermode. Esophageal evoked potentials (EEP) were recorded from the vertex following 200 electrical stimuli, and anterior chest wall evoked potentials (ACWEP) were recorded following 40 heat pulses. The fear of pain questionnaire (FPQ) was administered on V1. Statistical data are shown as point estimates of difference +/- 95% confidence interval. Pain thresholds increased between V1 and V3 [Eso-PT: V1-V3 = -17.9 mA (-27.9, -7.9) P < 0.001; ACW-PT: V1-V3 = -3.38 degrees C (-5.33, -1.42) P = 0.001]. The morphology of cortical responses from both sites was consistent and equivalent [P1, N1, P2, N2 complex, where P1 and P2 are is the first and second positive (downward) components of the CEP waveform, respectively, and N1 and N2 are the first and second negative (upward) components, respectively], indicating activation of similar cortical networks. For EEP, N1 and P2 latencies decreased between V1 and V3 [N1: V1-V3 = 13.7 (1.8, 25.4) P = 0.02; P2: V1-V3 = 32.5 (11.7, 53.2) P = 0.003], whereas amplitudes did not differ. For ACWEP, P2 latency increased between V1 and V3 [-35.9 (-60, -11.8) P = 0.005] and amplitudes decreased [P1-N1: V1-V3 = 5.4 (2.4, 8.4) P = 0.01; P2-N2: 6.8 (3.4, 10.3) P < 0.001]. The mean P1 latency of EEP over three visits was 126.6 ms and that of ACWEP was 101.6 ms, reflecting afferent transmission via Adelta fibers. There was a significant negative correlation between FPQ scores and Eso-PT on V1 (r = -0.57, P = 0.05). These data provide the first neurophysiological evidence of convergent esophageal and somatic pain pathways in humans.
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PMID:Neurophysiological evaluation of convergent afferents innervating the human esophagus and area of referred pain on the anterior chest wall. 2002 27

Esophageal pain that manifests as heartburn or chest pain, is a prevalent problem. Esophageal chest pain is most often caused by gastroesophageal reflux disease (GERD), but can also result from inflammatory processes, infections involving the esophagus, and contractions of the esophageal muscle. The mechanisms and pathways of esophageal chest pain are poorly understood. Vagal and spinal afferent pathways carry sensory information from the esophagus. Recently, esophageal hypersensitivity is identified as an important factor in the development of esophageal pain. A number of techniques are available to evaluate esophageal chest pain such as endoscopy and/or proton-pump inhibitor trial, esophageal manometry, a combined impedance-pH study, and esophageal ultrasound imaging. Proton pump inhibitors (PPIs) have the huge success in the treatment of GERD. Other drugs such as imipramine, trazadone, sertraline, tricyclics, and theophylline have been introduced for the control of esophageal chest pain in partial responders to PPI and the patients with esophageal hypersensitivity. Novel drugs which act on different targets are anticipated to treat esophageal pain in the future.
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PMID:[Diagnosis and management of esophageal chest pain]. 2038 74