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Controlling Pancreatitis Pain

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In patients with pancreatitis, treatments for the nervous system, rather than the pancreas itself, might better reduce pain, according to a study in the August issue of Clinical Gastroenterology and Hepatology.

Chronic pancreatitis is painful—surgery or endoscopy to reduce pressure in the parenchyma or in the pancreatic duct does not always relieve patients’ pain. Søren Schou Olesen et al. studied pain control in 25 patients with chronic pancreatitis and 15 healthy volunteers. Following an initial painful stimuli (holding a hand in ice-cold water), people normally have a much higher tolerance for subsequent painful stimuli (pressure to the quadriceps muscle)—this is known as descending pain modulation. Olesen et al. found that this process was defective in patients with pancreatitis; they were much more sensitive to the second painful stimulus than the healthy volunteers. The patients with chronic pancreatitis were also more sensitive to electrical and heat stimulation of the rectosigmoid colon.

The authors propose that recurrent pancreatic pain attacks might alter the way the central nervous system processes information about pain, making patients with pancreatitis more sensitive to stimuli. Similar effects have been observed in patients with irritable bowel syndrome and fibromyalgia.

The protocol used for the experiment. The cold pressor test is used as conditioning stimulus to induce descending pain inhibition (DNIC) in healthy volunteers and patients with chronic pancreatitis. Somatic pressure stimulations of the quadriceps muscle are used to quantify the effect of DNIC. To investigate central pain processing, multimodal (electrical, heat, and mechanical) stimulation of the rectosigmoid is performed. Simultaneous recordings of evoked brain potentials are obtained during the electrical stimulations of the rectosigmoid. Median nerve stimulations with simultaneous recordings of evoked brain potentials are performed to evaluate the presence of neuropathy in peripheral or central nervous pathways.

In an accompanying editorial, Peter Czakanski and Timothy Ness recommend that clinicians change their approach to patients with chronic pancreatitis; in addition to repairing damage to the pancreas, they should also address descending pain modulation from supraspinal structures and central nervous system sensitization using analgesics, anti-depressants, or anti-convulsant ion-channel inhibitors. Further experiments are required to determine whether impaired pain modulation is a cause or secondary effect of the pain associated with pancreatic inflammation.

More Information on Pancreatitis:

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Read the article online:
Olesen SS, Brock C, Krarup AL, et al. Descending inhibitory pain modulation is impaired in patients with chronic pancreatitis. Clin Gastroenterol and Hepatol 2010;8:724–730.

Read the accompanying editorial:
Czakanski P and Ness TJ. Impaired diffuse noxious inhibitory controls: an additional mechanism of pain in chronic pancreatitis? Clin Gastroenterol and Hepatol 2010;8:647–648.

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About The Author:

Dr. Kristine Novak

Dr. Kristine Novak

Dr. Kristine Novak is a science writer and editor based in San Francisco. She has extensive experience covering gastroenterology, hepatology, immunology, oncology, clinical, and biotechnology research discoveries.

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