Abstract
BackgroundImaging studies of bones in patients with sensory deficits are scarce.AimTo investigate bone MR images of the lower limb in diabetic patients with severe sensory polyneuropathy, and in control subjects without sensory deficits.MethodsRoutine T1 weighted and T2-fat-suppressed-STIR-sequences without contrast media were performed of the asymptomatic foot in 10 diabetic patients with polyneuropathy and unilateral inactive Charcot foot, and in 10 matched and 10 younger, non-obese unmatched control subjects. Simultaneously, a Gadolinium containing phantom was also assessed for reference. T1 weighted signal intensity (SI) was recorded at representative regions of interest at the peritendineal soft tissue, the tibia, the calcaneus, and at the phantom. Any abnormal skeletal morphology was also recorded.ResultsMean SI at the soft tissue, the calcaneus, and the tibia, respectively, was 105%, 105% and 84% of that at the phantom in the matched and unmatched control subjects, compared to 102% (soft tissue), 112% (calcaneus) and 64% (tibia) in the patients; differences of tibia vs. calcaneus or soft tissue were highly significant (p < 0.005). SI at the tibia was lower in the patients than in control subjects (p < 0.05). Occult traumatic skeletal lesions were found in 8 of the 10 asymptomatic diabetic feet (none in the control feet).ConclusionMR imaging did not reveal grossly abnormal bone marrow signalling in the limbs with severe sensory polyneuropathy, but occult sequelae of previous traumatic injuries.
Highlights
Neuro-osteoarthropathy of the feet, i.e. the Charcot foot in diabetes, is believed to be caused either by repeat traumatisation of an injured insensitive foot [1,2], or by a hypothetical neurogenic bone dystrophy [2,3], or both
MR imaging did not reveal grossly abnormal bone marrow signalling in the limbs with severe sensory polyneuropathy, but occult sequelae of previous traumatic injuries
signal intensity (SI) was significantly lower at the tibia in all three subject groups (p < 0.005); SI at the tibia was lower in the neuropathic patients than in control subjects (p < 0.05)
Summary
Neuro-osteoarthropathy of the feet, i.e. the Charcot foot in diabetes, is believed to be caused either by repeat traumatisation of an injured insensitive foot [1,2], or by a hypothetical neurogenic bone dystrophy [2,3], or both. The „diabetic“ Charcot foot might be caused by a specific osteopathy, or by an „abnormal“ reaction of the „diabetic bone“ to simple mechanical stress [4]. While it is undisputed that a most severe loss of protective sensation, and of pain sensation in particular [5], is a necessary prerequisite for a Charcot foot to develop, bone abnormalities consistent with a neuropathic osteopathy so far have not been demonstrated convincingly. Imaging studies of bones in patients with sensory deficits are scarce
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