Somatosensory profiling to differentiate distinct painful diseases of the pancreas—a quantitative sensory testing case-control study

Mechanisms of pancreatic pain are insufficiently understood, and quantitative sensory testing (QST) may help to identify the underlying mechanisms. Accordingly, this study assessed comprehensive somatosensory profiles encompassing nociceptive and nonnociceptive parameters in 70 patients with distinct pancreatic diseases, namely acute (n = 23), chronic (n = 20), or autoimmune pancreatitis (n = 10) and pancreatic cancer (n = 17) and compared it with 30 healthy control subjects by standardized QST (protocol of the German research network on neuropathic pain). Patients with pancreatic diseases presented significant somatosensory deficits in all thermal and tactile detection and pain thresholds in the pancreatic viscerotome (Th10), when compared with a remote control area (dermatome C5) or reference data of matched healthy controls ( P < 0.05- P < 0.0001). Unaltered vibration detection emphasizes the strictly regional character of losses. Loss of sensitivity paralleled the occurrence of paradoxical heat sensation (Th10 vs C5; P < 0.05), an indicator of thermal integration deficit. Punctate hyperalgesia or pain to light touch, the hallmark signs of spinal central sensitization were mostly absent and pain summation remained unchanged ( P > 0.05). Stratification of patients revealed that somatosensory deficits were significantly more pronounced in acute compared with chronic pancreatitis (eg, cold and warm detection thresholds: -2.19 ± 1.42 vs -1.10 ± 1.23 and -1.30 ± 1.68 vs -0.11 ± 1.80 z-values; P < 0.05 each). Notably, blunt pressure hyperalgesia, the only somatosensory parameter exhibiting significant gain compared with the patients' remote C5 segment, was a frequent finding only in acute, but not in chronic pancreatitis. The somatosensory phenotype of patients with distinct pancreatic disorders was characterized by a wide array of sensory losses being most severe in acute pancreatitis.

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Journal
Pain
Published
2025-04-04
DOI
https://doi.org/10.1097/j.pain.0000000000003601
Citations
3
Primary Topic
Pain Mechanisms and Treatments
Type
article
Field-Weighted Citation Impact
3.49
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article

Somatosensory profiling to differentiate distinct painful diseases of the pancreas—a quantitative sensory testing case-control study

Walter Magerl, Philipp Göltl, Michael Hirth, Matthias P. Ebert et al.
3 citations
Pain
Pain Mechanisms and Treatments
3.49
article

Somatosensory profiling to differentiate distinct painful diseases of the pancreas—a quantitative sensory testing case-control study

Walter Magerl, Philipp Göltl, Michael Hirth, Matthias P. Ebert, Paul Merz, Alexander Schneider
article en
3 citations

Abstract

Mechanisms of pancreatic pain are insufficiently understood, and quantitative sensory testing (QST) may help to identify the underlying mechanisms. Accordingly, this study assessed comprehensive somatosensory profiles encompassing nociceptive and nonnociceptive parameters in 70 patients with distinct pancreatic diseases, namely acute (n = 23), chronic (n = 20), or autoimmune pancreatitis (n = 10) and pancreatic cancer (n = 17) and compared it with 30 healthy control subjects by standardized QST (protocol of the German research network on neuropathic pain). Patients with pancreatic diseases presented significant somatosensory deficits in all thermal and tactile detection and pain thresholds in the pancreatic viscerotome (Th10), when compared with a remote control area (dermatome C5) or reference data of matched healthy controls ( P < 0.05- P < 0.0001). Unaltered vibration detection emphasizes the strictly regional character of losses. Loss of sensitivity paralleled the occurrence of paradoxical heat sensation (Th10 vs C5; P < 0.05), an indicator of thermal integration deficit. Punctate hyperalgesia or pain to light touch, the hallmark signs of spinal central sensitization were mostly absent and pain summation remained unchanged ( P > 0.05). Stratification of patients revealed that somatosensory deficits were significantly more pronounced in acute compared with chronic pancreatitis (eg, cold and warm detection thresholds: -2.19 ± 1.42 vs -1.10 ± 1.23 and -1.30 ± 1.68 vs -0.11 ± 1.80 z-values; P < 0.05 each). Notably, blunt pressure hyperalgesia, the only somatosensory parameter exhibiting significant gain compared with the patients' remote C5 segment, was a frequent finding only in acute, but not in chronic pancreatitis. The somatosensory phenotype of patients with distinct pancreatic disorders was characterized by a wide array of sensory losses being most severe in acute pancreatitis.

PainVol. 166(10)
Heidelberg University (DE), University Hospital Heidelberg (DE), Bernstein Center for Computational Neuroscience Heidelberg-Mannheim (DE), University Medical Centre Mannheim (DE)
Good health and well-being
Openalex Percentile: Top 8%
Pain Mechanisms and Treatments
3.49
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