Pressure pain perception in the diabetic Charcot foot: facts and hypotheses

Abstract

BackgroundReduced traumatic and posttraumatic (nociceptive) pain is a key feature of diabetic neuropathy. Underlying condition is a gradual degeneration of endings of pain nerves (A-delta fibers and C-fibers), which operate as receivers of noxious stimuli (nociceptors). Hence, the absence of A-delta fiber mediated sharp pain (“first” pain), and of C-fiber mediated dull pain (“second” pain). However, patients with diabetic neuropathy and acute Charcot foot often experience deep dull aching in the Charcot foot while walking on it.AimTo create a unifying hypothesis on the kind of pain in an acute Charcot foot.ResultAbsence of punctuate (pinprick) pain perception at the sole of a Charcot foot, as was shown recently, likely corresponds to vanished intraepidermal A-delta fiber endings. C-fiber nociceptors are reduced, according to histopathology studies. Both types of fibers contribute to posttraumatic hyperalgesia at the skin level, as studies show. Their deficiencies likely impact on posttraumatic hyperalgesia at the skin level and, probably, also at the skeletal level.ConclusionIt is hypothesised that deep dull aching in an acute diabetic Charcot foot may represent faulty posttraumatic hyperalgesia involving cutaneous and skeletal tissues.

Effect of painless diabetic neuropathy on pressure pain hypersensitivity (hyperalgesia) after acute foot trauma

“…All of these pitfalls and shortcomings in QST methodology and study design may have precluded statistical significance for many a group difference. Nevertheless, the data apparently support our previous hypothesis that abrogated cutaneous pressure pain perception might be more important than reduced deep pressure pain perception as a precondition for both types of neuropathic foot injuries (diabetic neuropathic ulcers or Charcot arthropathy) ( 10 , 22 , 34 ).…”

“…However, the nature of the deep pressure pain, as produced percutaneously by Algometer II ® , is generally not well understood. In the present case subjects, some of the intramuscular nociceptors/mechanoceptors inside m. abductor hallucis may have escaped neuropathic destruction, according to the distal-to-proximal gradient of neuropathy at the diabetic foot ( 34 ) (possibly also some intracutaneous nociceptors were preserved at the plantar arch, which remains to be demonstrated). Of these residual intramuscular nociceptors/mechanoceptors, some might have been captured and stimulated simultaneously by the relatively large contact area (1 cm 2 ) compressed.…”

Charcot foot syndrome

“…The neurological deficit in the distal neuropathy of diabetes is, however, very different: immediate sharp pain sensation is lost as a result of disruption of the ascending spinothalamic pathways, but deep pain sensation is typically intact. Many people with a Charcot foot in diabetes are aware of aching discomfort [20]. Similar inflammatory arthropathies have been described in association with a range of unrelated disorders and no common pattern has emerged to suggest the key involvement of any particular nerve pathway or fibre type.…”

Conventional deep pressure algometry is not suitable for clinical assessment of nociception in painless diabetic neuropathy

“…In conclusion, spatial summation of a multitude of low-threshold pressure receptors simultaneously activated by innocuous force during conventional pressure algometry explains the seeming discrepancy between absence of pinprick-perception and presence of deep pressure pain perception in persons with PLDN and painless foot ulcers. Our previous hypothesis is, thus, unlikely that ‘residual C-fibre nociceptors inside musculoskeletal structures may contribute to deep dull aching’ ( 3 ) as stimulated by Algometer II in feet with PLDN. Conventional deep pressure algometry is unsuitable for assessing nociceptive dysfunction at the diabetic foot.…”