Diabetic neuropathy should not be diagnosed solely on the basis of the vibration perception threshold, sural/radial amplitude ratio, and dorsal sural/radial amplitude ratio

Dear Sir,

We read with interest the article by Shaikh et al. on a cross-sectional study of the efficacy of sural/radial amplitude ratio (SRAR) and dorsal SRAR (DSRAR) in discriminating neuropathic (vibration perception threshold (VPT) >15) and non-neuropathic patients (VPT <15) with type 2 diabetes.^[1] The amplitudes of the sural and dorsal sural nerve were significantly lower in the neuropathic group than in the non-neuropathic group.^[1] The mean SRAR was higher in non-neuropathic participants than in patients with neuropathy.^[1] Similarly, DSRAR was reduced in the neuropathic group compared to patients without neuropathy.^[1] It was concluded that both SRAR and DSRAR have the diagnostic potential to detect diabetic neuropathy.^[1] The study is noteworthy, but some points should be discussed.

The first point is that the study group with neuropathy and the group without neuropathy were not matched in terms of age and height.^[1] As older and short people have lower amplitudes than younger and taller people,^[2] it would have been imperative to match the groups on these parameters.

The second point is that diabetic neuropathy usually starts with small fiber neuropathy (SFN) and not with large fiber neuropathy.^[3] Therefore, assessment of small fiber involvement (A-delta and C fibers) is more effective for the early diagnosis of diabetic neuropathy than sural and dorsal nerve conduction studies. SFN can be documented by several techniques, including quantitative sudomotor axon reflex testing (QSART), laser-evoked potentials, sympathetic skin response, confocal corneal microscopy, and skin biopsy.^[4]

The third point is that the average duration of diabetes was similar in patients with and without neuropathy, suggesting that factors other than disease duration are responsible for the development of neuropathy. Was diabetes less well controlled in patients with neuropathy compared to patients without neuropathy? Were hemoglobin A1c levels different in patients with and without neuropathy? How many of the included patients had diabetic myelopathy and how many had diabetic encephalopathy? Knowledge of these values is crucial as they can significantly influence the results of VPT.

The fourth point is that the presence or absence of diabetic neuropathy was assessed using the VPT. Since the detection of vibration in the brain depends not only on conduction along peripheral nerve fiber, but also on receptors, conduction through the dorsal column of the spinal cord, and processing of the signal in the brain, the diagnosis of diabetic neuropathy based on VPT alone may be misleading.

In summary, the study has limitations that affect the results and their interpretation. Addressing these limitations could strengthen the conclusions and support the message of the study. Sensory neuropathy of the sural nerve and dorsal sural nerve should not be diagnosed using the VPT alone, but by other, more reliable methods.