Per UpToDate, the key here is the allodynia. This patient has intact sensation, it's just "turned up" way too much. The simplest way to explain this is that the sensor itself (the nociceptor) is over-activated.
Note that nociceptive pain (as this is termed) is more often due to inflammation/pressure/tissue damage, whereas neuropathic pain (more central) has a wide variety of causes (diabetes is a prominent one).
Was I wrong to just pick the only answer with the word nociceptor in it?
the way I approached this was that the patient has intact vibration sense but has lost sensation to pinprick. if the lesion was in the dorsal root ganglia (a) or dorsal horn (b) or dorsal root afferents (d), the sensory loss would be more widespread than loss of one modality.
Allodynia is central pain sensitization. Triggering of pain by a non painful stimuli. Also seen in Fibromyalgia. [vs Hyperalgesia : Inc response to painful stimuli]
Its a positive (i.e Actively feeling, not lack of feeling) symptpms. so B & C is not the answer. D isnt answer either. as vanilloid receptor (TRPV1) is also afferent nociceptive transmission (modulated by capsaicin). Activation is soon followed by desensitization.
A - IDK. if problem was in DRG there would be lot more symptoms.
submitted by โseagull(1933)
Another approach. Diabetes causes non-enzymatic glycosylation which may negatively impact the function of neurons mainly due to altered blood supply among other things. These glycosylate deposits typically occur peripherally at the legs. The only peripheral answer choice was a nociceptor in the legs. all the other answer choices are at least more centrally located with larger blood supplies.
Again, not perfect but a way to reason out this answer but it does work.