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The medical literature presents diabetic sensory polyneuropathy as a length-dependent process producing a stocking distribution of sensory loss in the lower extremities. If a purely length-dependent etiology for diabetic sensory polyneuropathy were true, then a validated comparison of sensory loss at any equidistant site about the forefoot will reveal findings consistent with the accepted stocking pattern of anesthesia. A single-blinded, age-matched, control/experimental study is made into the frequency of apparent purely length-dependent A-beta fiber pathology in developing diabetic sensory polyneuropathy. Control (n = 46) and experimental (n = 83) central US subjects are examined with a subjective neuropathy screening questionnaire, vibratory threshold, and single-point pressure threshold testing. There is a plantar predominant pattern (61.5%) of sensory loss in developing diabetic sensory polyneuropathy, even after adjusting for sensitivity differences between different areas of the foot. A typical stocking pattern of sensory loss was not found. Although axonal pathology is length dependent, it is not apparently a purely length-dependent process. Therefore, a purely metabolic explanation for sensory loss is unlikely. In addition, an anatomic component for A-beta fiber pathology is implied by this study.
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