Comparing Michigan Neuropathy Screening Instrument Score with Plantar Sensory Nerve Conduction Study in Diabetic Neuropathy

By Saba Zaidi¹, Almas Zafar²

Affiliations

1. Department of Neurology, Liaquat National Hospital and Medical College, Karachi, Pakistan
2. Department of Internal Medicine, Abbasi Shaheed Hospital, Karachi, Pakistan

doi: 10.29271/jcpsp.2025.10.1241

ABSTRACT
Objective: To compare the Michigan Neuropathy Screening Instrument (MNSI) score and plantar sensory nerve conduction study (NCS) in diabetic patients with neuropathy.
Study Design: Comparative study.
Place and Duration of the Study: Department of Neurology, Liaquat National Hospital, Karachi, from March to August 2024.
Methodology: Using a non-probability purposive sampling technique, patients aged between 16 and 65 years with diabetic polyneuropathy and age-method healthy controls were included in the study. Neuropathy was graded based on MNSI score. Sural and plantar NCS were performed using the standard and modified Ponsford techniques, respectively. All evaluations were performed using a Nihon Kohden electromyography system to ensure reliable results. Data were collected using a well-designed questionnaire administered by neurology trainees and later analysed by SPSS version 27.
Results: A total of 78 participants, comprising 53 diabetic patients (33 MNSI-positive, 20 MNSI-negative) and 25 age-matched healthy controls, were analysed. MNSI-positive patients had significantly higher HbA1c and fasting blood sugar (FBS) levels compared to MNSI-negative patients with p = 0.005 and p = 0.001, respectively. The sural nerve conduction abnormalities were found in 39.7% participants, while 51.3% participants showed plantar nerve conduction abnormalities. There was a notable association between higher MNSI score and abnormal plantar NCS (p = 0.001), with significantly reduced amplitudes and conduction velocities in MNSI-positive patients, highlighting their sensitivity in detecting diabetic polyneuropathy. Additionally, lower amplitudes in the MNSI-negative group indicated their potential for identifying subclinical diabetic peripheral neuropathy (DPN).
Conclusion: The comparison of MNSI score with plantar sensory nerve conduction studies demonstrates that integrating both methods enhance the detection of early diabetic neuropathy.

Key Words: Diabetic peripheral neuropathy, Plantar nerve conduction studies, sural nerve conduction studies, Michigan Neuropathy Screening Instrument, Glycated haemoglobin.

INTRODUCTION

Despite being commonly used tests, nerve conduction study (NCS) shows normal results in 38–67% of patients suspected of having diabetic peripheral neuropathy (DPN).¹ The sural sensory nerve action potential (SNAP) is widely used in electrodiagnostic assessments to detect distal sensorimotor neuropathy, commonly seen in diabetic patients. However, because the sural nerve is not the most distal nerve in the foot, significant sensorimotor impairment in the feet may occur before changes in SNAP amplitude are observed electrophysiologically.^2-4

For the early detection of peripheral neuropathy, the literature favours assessing more distal mixed sensory and motor nerves, such as the medial and lateral plantar nerves.^5-7 In 1984, Reeves et al. were the first to propose that the medial plantar nerve could serve as a sensitive marker for detecting early diabetic peripheral neuropathy.⁷ Originating from the tibial nerve along with the lateral plantar nerve, the medial plantar nerve innervates the medial aspect of the sole, including the toes. It provides crucial sensory input, which is essential for detecting subtle neuropathic changes that might be missed by routine NCS.

The study aimed to extend routine NCS by incorporating plantar nerve assessment using the Pornsfield method in patients with DPN. Additionally, the Michigan neuropathy screening instru-ment (MNSI) score was used for the clinical assessment of neuropathy.

METHODOLOGY

This comparative, analytical study was conducted at the Department of Neurology, Liaquat National Hospital, Karachi, Pakistan, from March to August 2024. Ethical approval was obtained from the Ethical Review Committee of the hospital (Ref. No. 1151-2024-ERC-LNH). After obtaining informed consent from all participants, data collection was carried out by neurology trainees using a well-structured questionnaire over a period  of  six  months.

The MNSI score consists of two parts: one performed by a patient and the other is performed by a health professional. The health professional part of the MNSI includes a brief physical examination, which involves examining the feet for deformities, dry skin, abnormalities in hair or nails, calluses, or signs of infection; assessing vibration sensation semi-quantitatively on the dorsum of the great toe; grading ankle reflexes; and performing monofilament testing. Patients scoring more than 2 points on this 10-point scale in the clinical portion of the MNSI are considered to have neuropathy and are referred for further evaluation. Diabetic participants were divided into MNSI-positive (>2.5) and MNSI-negative (<2.5) groups based on their scores.

The sample size was calculated using the mean ± standard deviations (SD) of the plantar nerve action potential amplitude: 0.79 ± 0.84 for the asymptomatic diabetic group (MNSI-negative), 1.23 ± 0.9 for the symptomatic diabetic group (MNSI-positive), and 1.71 ± 0.84 for the control group. The calculation was performed using PASS software, with a test power of 90% and a 95% confidence interval. The total required sample size was 78 patients, with 26 participants in each group. However, due to recruitment limitations, the final sample comprised 33 participants in one group, 20 in another, and 25 in the control group.

The inclusion criteria included patients aged 16-65 years diagnosed with diabetic neuropathy, excluding individuals with other causes of neuropathies, such as those associated with other endocrine disorders or medicines, radiculopathy, or medial plantar neuropathy due to local causes such as tarsal tunnel syndrome or trauma. Individuals aged above 65 years were excluded to minimise the influence of age-related declines in medial plantar amplitudes, which could complicate the interpretation of nerve conduction results and further analysis. Control participants consisted of age-matched non- diabetic individuals, providing a baseline comparison for medial plantar sensory NCS. After obtaining patient consent, the following information was recorded: demographic details, duration of diabetes, comorbidities, current medications, as well as the most recent blood sugar values and glycated haemoglobin levels. NCS were conducted using standard surface stimulation and recording techniques with an electromyography device and standard filter settings. Routine NCS included motor and sensory nerve conduction for the median and ulnar nerves, sensory nerve conduction for the bilateral sural nerves, and motor nerve conduction for the peroneal nerve. The medial plantar sensory NCS was performed by stimulating the medial plantar nerve using surface electrodes placed on the great toe, with an active surface electrode placed  above  the  flexor  retinaculum.

The surface skin temperature of the foot was maintained at 32°C, and the resulting waveforms were averaged by the machine to extract the true signal. Abnormal medial plantar sensory NCS was defined as values deviating by ±2 SD from the mean of the control group. Quantitative median plantar sural sensory nerve action potential (MP SNAP) values were evaluated against age-matched normal values. If the nerve could not be stimulated after two attempts, it was considered unrecordable, and the amplitude was documented as zero.

The Chi-square test was used to compare demographic data with MNSI score, the Mann-Whitney U test was applied quantitative diabetic values such as HbA1c and fasting blood sugar (FBS), and the Kruskal-Wallis test was employed to compare electrophysiological values between the disease and control groups. Normality of continuous variables was assessed using the Shapiro-Wilk test and the Kolmogorov-Smirnov test. A p-value of less than 0.05 was considered statistically significant.

RESULTS

A total of 78 participants were included in the study. Among them, 53 were diabetic patients, with 33 categorised as MNSI- positive and 20 as MNSI-negative. Additionally, 25 age-matched healthy controls were included. Although individuals with age over 65 years were excluded, the majority of participants (n = 64, 82.1%) were above 50 years of age. Diabetes duration of up to 5 years was observed in 24 (30.8%) of the study population. Hypertension (HT) was present in 15 (19.2%), while 2 (2.6%) had ischaemic heart disease (IHD). Sural nerve conduction abnormalities were detected in 31 participants (39.7%), whereas 47 (60.3%) had normal sural nerve conduction out of 78 participants. In contrast, plantar NCS were abnormal in 40 participants (51.3%), while 38 (48.7%) had normal findings. The detailed demographic characteristics of the study participants are presented in Table I.

The association between demographic factors and study participants was analysed using the Chi-square test and the Mann-Whitney U test. Age, gender, HT, and IHD did not show statistically significant associations with the MNSI-positive group, with p-values of 0.536, 0.167, 0.270, and 0.617, respectively. However, diabetes duration demonstrated a statistically significant association, with a p-value of 0.007.

Table  I:  Demographic  characteristics  of  the  study  participants.

Variables	No. of participants	Results
Age >50 years	78	64 (82.1%)
Women		41 (52.6%)
Duration of diabetes
<1 year		6 (7.7%)
1-5 years		24 (30.8%)
6-10 years		14 (17.9%)
11-20 years		9 (11.5%)
Co-morbidities
HT		15 (19.2%)
IHD		2 (2.6%)
Neuropathy category based on MNSI score
No neuropathy (MNSI score <2.5)	53	33 (62.2%)
Neuropathy (MNSI score >2.5)		20 (37.7%)
IHD: Ischaemic heart disease; HT: Hypertension; MNSI: Michigan neuropathy screening instrument. Values are given as frequency n (%).

Table II: Association of demographic and neurophysiological parameters in the study participants.

Variables		Diabetic patients		p-values
		MNSI-positive Group	MNSI-negative Group
Age years	<50 years	4	3	0.536
	>50 years	29	17
Diabetes duration in years	<1 year	3	3	0.007*
	1-5 years	11	13
	6-10 years	10	4
	11-20 years	9	0
Gender	Male	18	7	0.167
	Female	15	13
HT	Yes	7	7	0.27
	No	26	13
IHD	Yes	1	1	0.617
	No	32	19
Recent HbA1c		7.5	7.6	0.005**
FBS		23	12.75	0.001**
Sural nerve	Sural normal	20	10	0.45
	Sural abnormal	13	10
Plantar sensory study	Normal	3	11	0.001*
	Abnormal	30	9
H reflex	Normal	14	15	0.021*
	Poorly modulated	19	5
*p <0.05 is significant using the Chi-square test, **p <0.05 is significant using the Mann-Whitney U test. IHD: Ischaemic heart disease, HT: Hypertension; MNSI: Michigan neuropathy screening instrument.

Table III: Results of NCS of sural and medial plantar nerves in three groups.

Nerves	MNSI-positive Group	MNSI-negative Group	Control Group	p-values
Right medial plantar	-	-	-	-
Amplitudes in microvolts	0.0 (0.0)	3.95 (17.3)	14.0 (12.3)	<0.001*
Conduction velocity in m/s	0.0 (0.0)	21.0 (50.3)	43.0 (8.4)	<0.001*
Left medial plantar	-	-	-	-
Amplitudes in microvolts	0.0 (0.0)	5.30 (17.8)	14.0 (11.1)	<0.001*
Conduction velocity in m/s	0.0 (0.0)	20.5 (24.3)	43 (14.5)	<0.001*
Right lateral plantar	-	-	-	-
Amplitudes in microvolts	0.0 (0.0)	4.30 (17.0)	12 (8.7)	<0.001*
Conduction velocity in m/s	0.0 (0.0)	20.5 (47.0)	44 (8.0)	<0.001*
Left lateral plantar	-	-	-	-
Amplitudes in microvolts	0.0 (0.0)	5.0 (18.1)	15.0 (10.8)	<0.001*
Conduction velocity in m/s	0.0 (0.0)	19.75 (47.8)	42.0 (9.5)	<0.001*
Right sural	-	-	-	-
Amplitudes in microvolts	0.0 (12.6)	16.0 (14.9)	17.20 (11.5)	<0.001*
Conduction velocity in m/s	0.0 (38)	43.0 (8)	41.0 (8)	<0.001*
Left sural	-	-	-	-
Amplitudes in microvolts	0.0 (12.5)	16.5 (16.3)	18.0 (10.4)	<0.001*
Conduction velocity in m/s	0.0 (35.8)	42.5 (5.3)	43.0 (6.5)	<0.001*
*Statistically significant at p <0.05. Results are presented as median (IQR), the Kruskal-Wallis test was applied.

Furthermore, when comparing glycaemic control indicators between the two groups, there were significant differences in both recent HbA1c and FBS levels. MNSI-positive patients had a higher median HbA1c (7.5) than MNSI-negative patients (7.6), with a significant p-value of 0.005. Additionally, FBS was higher in the MNSI-positive group (23) compared to the MNSI-negative group (12.75), with a p-value of 0.001. Nerve conduction findings showed the plantar sensory study (p = 0.001) was significantly associated with a high MNSI score. A poorly modulated H reflex also showed a significant association (p = 0.021). In contrast, sural sensory nerve abnormalities are not statistically significant (p = 0.45), as shown in Table II.

A comparative analysis of NCS between the disease and control groups is shown in Table III.

In the control group, plantar studies could not be performed for a single participant due to technical difficulties. In the diseased group, 16 patients had both sural and plantar responses that were non- recordable, while 21 had only non-recordable plantar responses.

For the right medial plantar nerve, the median amplitude in the MNSI-positive group was 0.0 µV (IQR: 0.0-27.0 µV), markedly lower than the MNSI-negative group (3.95 µV [IQR: 0.0-38.0 µV]) and the control group (14.0 µV [IQR: 0.0-41.0 µV]). Similarly, the median conduction velocity was significantly lower in the MNSI-positive group (0.0 m/s [IQR: 0.0-50.2 m/s]) compared to the MNSI-negative group (21.0 m/s [IQR: 0.0-56.0 m/s]) and the control group (43.0 m/s [IQR: 0.0-61.0 m/s]).

A comparable pattern was observed in the left medial plantar nerve, where the median amplitude and conduction velocity were the lowest in the MNSI-positive group (0.0 µV [IQR: 0.0-28.8 µV]), followed by the MNSI-negative group (5.30 µV [IQR: 0.0-40.0 µV]), and the highest values in the control group (14.0 µV [IQR: 0.0-39.0 µV]). Similarly, conduction velocities were significantly reduced in the MNSI-positive group (0.0 m/s [IQR: 0.0-42.0 m/s]) compared to the MNSI-negative group (20.5 m/s [IQR: 0.0-52.0 m/s]) and the control group (43.0 m/s [IQR: 0.0-55.0 m/s]).

The right lateral plantar nerve also showed a significant decline in the MNSI-positive group (0.0 µV [IQR: 0.0-20.0 µV]) compared to the MNSI-negative group (4.30 µV [IQR: 0.0-30.0 µV]) and the control group (12.0 µV [IQR: 0.0-28.0 µV]). Similarly, conduction velocity in the right lateral plantar nerve was significantly lower in the MNSI-positive group (0.0 m/s [IQR: 0.0-59.3 m/s]) compared to the MNSI-negative group (20.5 m/s [IQR: 0.0-59.0 m/s]) and the control group (44.0 m/s [IQR: 0.0-56.0 m/s]).

The left lateral plantar nerve followed the same trend, with the MNSI-positive group showing significantly lower amplitudes (0.0 µV [IQR: 0.0-17.4 µV]) and conduction velocities (0.0 m/s [IQR: 0.0-57.0 m/s]) compared to the MNSI-negative group (5.0 µV [IQR: 0.0-31.0 µV]) and the control group (15.0 µV [IQR: 0.0-33.0 µV]). Conduction velocities were also significantly lower in the MNSI-positive group compared to the MNSI-negative and control groups.

Similarly, in the right sural nerve, the median amplitude in the MNSI-positive group was 0.0 µV (IQR: 12.6-21.0 µV) and conduction velocity was 0.0 m/s (IQR: 38.0-50.0 m/s) compared to the MNSI-negative group (amplitude: 16.0 µV [IQR: 0.0-43.0 µV]; conduction velocity: 43.0 m/s [IQR: 0.0-61.0 m/s]) and the control group (amplitude: 17.20 µV [IQR: 6.4-35.0 µV]; conduction velocity: 41.0 m/s [IQR: 35.0-50.0 m/s]).

The left sural nerve exhibited the same pattern, with significantly reduced amplitudes (0.0 µV [IQR: 12.5-28.6 µV]) and conduction velocities (0.0 m/s [IQR: 35.8-49.0 m/s]) in the MNSI-positive group compared to the MNSI-negative group (amplitude: 16.5 µV [IQR: 0.0-38.0 µV]; conduction velocity: 42.5 m/s [IQR: 0.0-52.0 m/s]) and the control group (amplitude: 18.0 µV [IQR: 7.1-51.0 µV]; conduction velocity: 43.0 m/s [IQR: 35.0-55.0 m/s]).

In summary, the plantar nerve studies demonstrated a significant decline in both amplitudes and conduction velocities in the MNSI-positive group compared to the control group, highlighting their potential as sensitive markers for detecting diabetic neuropathy. Additionally, the lower amplitudes observed in the MNSI-negative group compared to the control group suggest that these studies may also help identify subclinical cases of DPN, even when routine clinical screening does not indicate neuropathy.

DISCUSSION

In this study, NCS findings revealed a notable difference in diagnostic yield between the sural nerve and plantar studies. Among the 33 MNSI-positive patients, 13 (39.4%) demonstrated sural nerve abnormalities, while 30 (90.9%) had abnormal plantar studies. These results showed the potential value of incorporating plantar sensory nerve conduction into the routine NCS protocol for neuropathy. A study appreciated the contribution of Reeves et al. who in 1984, proposed that medial plantar nerves can be assessed in diabetic neuropathy.⁷ Since then, limited studies have been conducted to establish the sensitivity of MP SNAP in diagnosing early diabetic neuropathy.^7-9

Burning feet sensation, commonly reported in DPN, is primarily attributed to small unmyelinated fibre damage, which is an early pathological change in DPN. The medial plantar nerve, responsible for sensory innervation of the plantar aspect of the foot, contains a mix of small and large fibres, making it particularly susceptible to early axonal degeneration.¹⁰ Diagnostic tests, such as measuring intraepidermal nerve fibre density, quantitative sensory testing (QST), and autonomic function testing, are available, but they can be invasive, complex, or difficult to interpret. Routine NCS are not designed to assess small fibre function and may miss early signs of DPN, particularly in the feet. Similarly, advanced neurophysiological techniques, including cutaneous silent period, sympathetic skin response, and thermal threshold testing, can assess small fibre involvement; however, these techniques require specialised equipment and expertise. In contrast, simple measurement of plantar nerve conduction may offer a practical, accessible alternative for evaluating diabetic neuropathy.¹¹

Most of the participants in this study were over 50 years of age; however, participants above 65 years were excluded due to the increased likelihood of false-negative results on plantar nerve conduction studies, which can occur due to age-related peripheral nerve changes. Comparatively, more female participants were present in this study, which might be due to higher prevalence of diabetic neuropathy-related symptoms among females in this age group or possibly due to selection bias. The distribution of diabetes duration among participants indicates a noteworthy trend. Most cases (n = 24, 30.8%) had a diabetes duration of 1–5 years, which may reflect the early onset of diabetic neuropathy symptoms or the increased likelihood of symptom detection within this time frame. Interestingly, 6 (7.7%) of participants had diabetes for less than 1 year, suggesting that neuropathy can develop relatively soon after diagnosis, possibly due to undiagnosed hyperglycaemia before formal diabetes diagnosis. On the other hand, 14 (17.9%) of participants with 6–10 years of diabetes and 9 (11.5%) with 11–20 years of diabetes suggest a progressive accumulation of cases as the disease duration increases. This trend reinforces the importance of regular neuropathy screening across all stages of diabetes, regardless of duration.^12-15

A statistically significant difference in HbA1c and FBS levels between the groups affirms the already well-established association between poor glycaemic control and the presence of neuropathy. This finding highlights the critical role of maintaining optimal glycaemic levels in preventing or delaying the onset of diabetic neuropathy, as already described in the prior literature.^16-20

The strengths of this study include the case-comparative study design, which allows for a direct comparison between diabetic patients and healthy controls, enhancing the reliability of the study findings. Additionally, plantar NCS were compared with actual control data rather than normative values, providing a more clinically relevant assessment of nerve dysfunction. Furthermore, appropriate statistical tools were employed to ensure the accuracy and robustness of the analysis, strengthening the validity of the results. One of the limitations of this study was that all participants had established diabetes, and other potential contributors to small fibre neuropathy — such as vitamin deficiencies, alcohol use, or medication effects (e.g., metformin-associated B12 deficiency) — were not systematically excluded. This should be considered when interpreting the association of small fibre neuropathy with medial plantar sensory NCS abnormalities in this cohort. In future, it is recommended to increase the sample size to enhance statistical power, which may improve the likelihood of detecting significant differences, especially in groups with non-recordable results. Additionally, a longitudinal study design will provide valuable insights into the progression of neuropathy over time, allowing for a better understanding of how early-stage changes evolve and increase the chances of obtaining measurable NCS values even in patients with advanced diabetes. By combining these approaches, future studies can yield more robust and meaningful findings.

CONCLUSION

The plantar sensory NCS in combination with the MNSI score offers greater diagnostic value than the sural NCS, enhanc-ing the early detection of diabetes.

ETHICAL APPROVAL:
Ethical approval was obtained from the Ethical Review Committee of the Liaquat National Hospital, Karachi, Pakistan (Ref. No. 1151-2024-ERC-LNH).

PATIENTS’ CONSENT:
Informed consent was obtained from all participants.

COMPETING INTEREST:
The authors declared no conflict of interest.

AUTHORS’ CONTRIBUTION:
SZ, AZ: Conception, acquisition, analysis, interpretation, and drafting.
Both authors approved the final version of the manuscript to be published.
 

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