Descending Inhibitory Pain Modulation Is Impaired in Patients With Chronic Pancreatitis

Olesen, Søren Schou; Brock, Christina; Krarup, Anne Lund; Funch‐Jensen, Peter; Arendt-Nielsen, Lars; Wilder‐Smith, O. H. G.; Drewes, Asbjørn Mohr

doi:10.1016/j.cgh.2010.03.005

Cited by 118 publications

(102 citation statements)

References 28 publications

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“…Therefore, the present easier applicable design has been developed and implemented in numerous studies. The maximum tolerated temperatures in the healthy subjects included in our study are between those found for healthy subjects by Olesen et al 28 and…”

Section: Discussionsupporting

confidence: 64%

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Rectal Mechano-sensory Function in Patients with Carcinoid Diarrhea

Gregersen

Brock

Haase

et al. 2016

J Neurogastroenterol Motil

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Background/AimsIn patients with neuroendocrine tumors, excessive production of serotonin and other amines may cause the carcinoid syndrome, which is mainly characterized by diarrhea and flushing. Little is known about the pathophysiology of carcinoid diarrhea. In several other groups of patients, diarrhea may be associated with rectal hypersensitivity and increased rectal tone. Therefore, the aim of the present study was to compare rectal sensitivity and compliance in patients with carcinoid diarrhea and in healthy subjects. MethodsTwelve patients (6 males, aged 54-78 years, median 65 years), with carcinoid diarrhea and 19 healthy subjects (7 males, aged 50-78 years, median 61 years) were included. Rectal mechanical and heat stimulation was used for assessment of rectal mechano-sensory properties. ResultsOverall, 5.3% higher temperatures were needed to elicit sensory responses in patients with carcinoid diarrhea than in healthy subjects (P = 0.015). Posthoc analyses revealed that the sensory threshold to heat was 48.1 ± 3.1 o C in patients vs 44.7 ± 4.7 o C in healthy subjects (P = 0.041). In contrast, patients and healthy subjects showed no overall differences in rectal sensory response to mechanical distension (P = 0.731) or rectal compliance (P = 0.990). ConclusionsPatients with carcinoid diarrhea have higher sensory thresholds to heat stimulation in comparison to healthy subjects, but normal rectal sensation to mechanical distension and normal compliance. Therefore, treatment of carcinoid diarrhea should aim at prolonging gastrointestinal transit and decreasing secretion, rather than modifying rectal mechano-sensory function.

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Section: Discussionsupporting

confidence: 64%

“…Data from 14 healthy subjects have been used in other studies. [27][28][29] Five patients had been part of a previous study on GI transit times in patients with carcinoid diarrhea. 15 The study was conducted in accordance with the Declaration …”

Section: Patients and Healthy Subjectsmentioning

confidence: 99%

Rectal Mechano-sensory Function in Patients with Carcinoid Diarrhea

Gregersen

Brock

Haase

et al. 2016

J Neurogastroenterol Motil

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“…While, the focus of pain origin in CP historically has been on the pancreatic gland, assuming pain to originate in the pancreas or its surrounding organs, recent findings indicate that both peripheral and central pain processing are abnormal in CP patients [1,3] . Various mechanisms responsible for the altered pain processing have been proposed, including pancreatic neuropathy and neural remodeling [4,5] , sensitization of neurons in the spinal cord and the brain [6,7] , reorganization of the brain areas involved in visceral pain processing [8] and alterations in descending pain control from the brainstem and other supraspinal structures [9] . The diagnostic work up of patients with painful CP should therefore not only focus on pancreatic and extra pancreatic causes of pain (e.g., pseudocysts, duct dilation and strictures, pancreatic head mass, etc.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiology as a tool to unravel the origin of pancreatic pain

Lelic

Olesen

Graversen

et al. 2014

WJGP

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Intense abdominal pain is the most common symptom in chronic pancreatitis, but the underlying mechanisms are not completely understood and pain management remains a significant clinical challenge. The focus of pain origin in chronic pancreatitis traditionally has been on the pancreatic gland, assuming pain to originate in the pancreas or its surrounding organs. However, research in the last decade points to abnormal central nervous system pain processing. For this reason, electroencephalography has been receiving increasing attention. In contrast to imaging methods such as functional magnetic resonance imaging and positron emission tomography, electroencephalogram has excellent temporal resolution making it possible to investigate central processing of pain on a millisecond time scale. Moreover, continuously advancing methodology made it possible to explore brain sources responsible for generation of evoked potentials and hence to study brain reorganization due to pain in chronic pancreatitis. The aim of this review is to give an overview of the current methods and findings in electroencephalography as a tool to unravel the origin of pancreatic pain.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Chronic pancreatitis; Electrophysiology; Evoked potentials; Brain source localization; Electroencephalography frequency analysis; Visceral pain; Chronic pain; Pancreatic pain Core tip: Chronic pancreatitis (CP) is a disease with progressive destruction of the pancreatic gland and intense abdominal pain is one of its main characteristics. The understanding of pain in CP has conventionally focused on the diseased pancreas itself, assuming pain to be due to increased parenchymal or ductal pressure. However, recent research points to possible involvement of abnormal central nervous system pain processing. This review gives an insight into electrophysiology as a tool to unravel brain abnormalities underlying pancreatic pain and provides up to date electrophysiological results in this patient group.

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“…In one study, increased areas of referred pain to electrical stimulation of the esophagus, stomach, and duodenum (sharing spinal segmental innervations with the pancreas and thus serving as proxies of true pancreatic simulation) was reported in CP patients compared to controls (21). Other studies reported decreased pain thresholds to visceral stimulation of the rectosigmoid as well as somatic stimulation of muscle and bone (7,46) and such hyperalgesia seems to be linked to disease severity in CP patients (3). Taken together, these findings characterise a generalised hyperalgesic state of the pain system and likely mirrors widespread sensitisation of the central nervous system as seen in many other chronic pain disorders (57).…”

Section: Central Sensitisationmentioning

confidence: 98%

“…Thus, several studies, both animal and human, have documented the involvement of brainstem structures in the generation and maintenance of central sensitisation and hyperalgesia (34,62). In the context of pain and CP, impaired descending inhibitory pain modulation has been reported in studies based on experimental human pain models (3,46). In addition, brainstem facilitation was reported to maintain pancreatic pain in an animal model of CP (55).…”

Section: Impaired Pain Modulationmentioning

confidence: 99%