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Clinical Neurophysiology 119 (2008) 880–885

Medial plantar and dorsal sural nerve conduction studies increasethe sensitivity in the detection of neuropathy in diabetic patients q,qq

Kayihan Uluc a,*, Baris Isak a, Deniz Borucu a, Cagri Mesut Temucin b,Yilmaz Cetinkaya c, Pinar Kahraman Koytak a, Tulin Tanridag a, Onder Us a

a Marmara University Hospital, Department of Neurology, Tophanelioglu Cad. 13/15 Altunizade, 34640 Istanbul, Turkeyb Hacettepe University, Institute of Neurological Sciences and Psychiatry, Ankara, Turkey

c Haydarpasa Numune Training and Research Hospital, Department of Neurology, Istanbul, Turkey

Accepted 2 January 2008

Abstract

Objective: Clinical utility of nerve conduction studies (NCS) of the medial plantar and dorsal sural nerves in the early detection ofpolyneuropathy have already been shown separately. However, at present, there is no data about the combined assessment of thesetwo nerves in distal sensory neuropathy. In the present study, we aimed to evaluate the medial plantar and dorsal sural NCS in a groupof diabetic patients with distal sensory neuropathy (DSN) and in healthy controls.Methods: Thirty healthy and 30 diabetic adult patients were included. In all subjects, peripheral motor and sensory NCS were performedbilaterally with surface electrodes on the lower limbs including medial plantar and dorsal sural nerves. In addition, motor and sensorynerves were studied unilaterally on the upper limb.Results: In all patients, nerve action potential (NAP) amplitudes of sural and superficial peroneal nerves were within normal ranges, butin the patient group mean value was significantly lower than in the controls. Among clinically defined 30 DSN patients, medial plantarNAP amplitude was abnormal in 18 (60%) and dorsal sural nerve amplitude was abnormal in 13 (40%) of the patients bilaterally. Addi-tionally, the onset NCV of the dorsal sural nerve was significantly slower in patients than controls (P = 0.038). Evaluation of both ofthese nerves increased the sensitivity up to 70% in the detection of neuropathy.Conclusions: Bilateral NCS assessment of both of the medial plantar and dorsal sural nerves together increases the rate of diagnosis ofdiabetic distal sensory neuropathy compared to assessment of either of these nerves.Significance: Assessment of medial plantar in addition to dorsal sural NCS together increases the sensitivity in the detection ofneuropathy and allows earlier diagnosis, especially when routine NCS are normal.� 2008 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Keywords: Medial plantar nerve; Dorsal sural nerve; Diabetic sensory neuropathy

1. Introduction

Distal sensory polyneuropathy (DSN) is a commondisorder (Wolfe et al., 1999; Herrmann et al., 2004) and

1388-2457/$34.00 � 2008 International Federation of Clinical Neurophysiolog

doi:10.1016/j.clinph.2008.01.001

q The study was performed in the neurophysiology laboratory atMarmara University Hospital.qq None of the authors has any direct or indirect conflicts of interest,financial or otherwise, relating to the subject of our report.

* Corresponding author. Tel.: +90 216 3271010/266; fax: +90 216325977.

E-mail address: kayihanu@yahoo.com (K. Uluc).

may involve small-myelinated and unmyelinated nervefibers, large-myelinated fibers, or both. Patients withDSN generally present with symmetrical painful dysesthe-sias including burning or lightening pains and numbnessin the feet and lower legs. DSN may be classified intothree forms (Nodera et al., 2002): small fiber neuropathy(SFN), mixed small and large-fiber sensory neuropathy(MFN) and large fiber neuropathy (LFN). While abnor-malities on pinprick or thermal testing are the signs ofSFN, LFN is characterized by abnormalities of proprio-ception, vibratory sensation or tendon reflexes with

y. Published by Elsevier Ireland Ltd. All rights reserved.

K. Uluc et al. / Clinical Neurophysiology 119 (2008) 880–885 881

normal strength and pinprick sensation. MFN requiresfeatures of both SFN and LFN. Apart from clinical signsand symptoms, nerve conduction studies (NCS) have animportant value in the diagnosis. As a part of thedying-back phenomenon, sensory nerves in the feet areusually affected in the early stages of polyneuropathy(Oh et al., 2001; Park et al., 2003; Singleton, 2005). Rou-tine NCS of sural and superficial peroneal nerves that arecommonly assessed for polyneuropathy have a limitationas they cannot evaluate the distal parts of the feet (Killianand Foreman, 2001). In contrast, medial plantar and dor-sal sural nerves which are estimated as the most distalsensory nerves of the feet may be affected in the earlystages of polyneuropathy. In recent reports, clinical utilityof NCS of the medial plantar and dorsal sural nerves inthe early diagnosis of polyneuropathy has been shownseparately (Løseth et al., 2007; Herrmann et al., 2004;Nodera et al., 2002; Killian and Foreman, 2001; Turgutet al., 2004; Balci et al., 2005). However, at present, wedo not have any data about the assessment of both ofthese two nerves together in DSN (Oh, 2007).

The main purpose of this study was to evaluate bothof the medial plantar and dorsal sural NCS in a groupof patients with diabetes mellitus (DM) with sensorysymptoms and signs and compare the results withhealthy controls. In addition, the results were comparedwith routine NCS evaluated in sural and superficialnerves, and with clinical symptoms and signs of polyneu-ropathy in the patient group.

2. Subjects and methods

2.1. Subjects

Thirty consecutive diabetic patients with clinically diag-nosed DSN and 30 healthy age- and sex-matched controlswere included in the study. To eliminate any concernabout the age effects on the NCS, patients under theage of 60 were included. Patients from the diabetic outpa-tient clinic presenting with symmetrical pain and/ornumbness in the feet plus one or more objective clinicalfindings suggesting of SFN, MFN or LFN were recruited.Neuropathic impairment score (NIS) of the lower limbs(LL)) was applied to each patient to grade neuropathicsigns (Bril, 1999). According to the neurological and elec-trophysiological examinations, patients with radiculopa-thy, mononeuropathy or plexopathy were excluded fromthe study.

Normative data for electrophysiological studies werederived from 30 healthy volunteers under 60 years of agewho had no risk factors for neuropathy and no abnormal-ities in neurological examination.

The study protocol was in accordance with the Hel-sinki declaration of human rights, and was approvedby the local Ethics Committee and all patients and con-trols gave written informed consent to participate in thestudy.

2.2. Electrophysiological investigations

2.2.1. Conventional motor and sensory nerve conduction

studies

Two investigators who were blinded to patient andcontrol groups assessed all of the electrophysiologicalstudies. For routine motor and sensory NCS, methodsthat were suggested by Falck et al. (1994) and Stalbergand Falck (1993) were used. In all patients and controls,bilateral posterior tibial, common peroneal motor nervesand bilateral sural and superficial peroneal sensorynerves with left median, ulnar motor and sensory nerves,and left radial sensory nerves were studied with a Mede-lec Synergy electromyography machine. Surface barrecording and bipolar surface recording electrodes (TecaCorp.) were used in the NCS. Standard antidromic meth-ods were used in the sural, superficial peroneal, median,ulnar and radial sensory NCS. In case of suspected CTS,bilateral median motor and sensory studies were per-formed. Compound muscle action potential (CMAP)amplitude, distal latency, conduction velocity and mini-mum F-response latency and F-wave persistence werecalculated for the motor NCS. Minimum F-responselatency was obtained using 20 stimulations. Onset andpeak latency, onset and peak nerve conduction velocity(NCV) and amplitude were measured for the sensoryNCS in the upper and lower extremities. The latencywas measured to the onset of the first negative deflectionand to the negative peak. NCV was calculated using theonset and peak latencies. Amplitude of the sensory NAPwas measured from the baseline to the negative peak.The pattern was accepted as an ‘‘absent NAP” if therewas no recognizable NAP or NAP was not repeatableand constant.

An average was used for all sensory nerve recordings,and the number of averages required to clearly define thepotential was 8. In order to obtain the maximum sensoryNAP, the stimulus intensity was supramaximal, i.e. at least3 times the sensory threshold. Filter settings were 5 Hz–10 kHz for motor studies and 20 Hz–2 kHz for sensorystudies. Skin temperature was maintained between 31 and34 �C in all subjects.

2.2.2. Medial plantar and dorsal sural nerve recordings

Medial plantar and dorsal sural nerve action potentialswere recorded bilaterally by the same surface bar recordingelectrodes (Teca Corp.) that were used in the other NCS.Standard sensory nerve conduction setup was used. Forthe medial plantar mixed nerve study, the medial solewas stimulated, and the NAP was recorded over the tibialnerve above and posterior to the medial malleolus at a dis-tance of 140 mm (Fig. 1) (Falck et al., 1994). To avoidinterference by a volume-recorded motor response, themethods that were previously published were used (Noderaet al., 2002). Following the stimulation of the distal portionof the medial sole, we observed for a toe flexor twitch, andlater, by using the lowest stimulus duration and intensity

Fig. 1. Medial plantar nerve conduction technique and a medial plantar SNAP recording from a control subject (S, stimulating electrode; R, recordingelectrode; G, ground electrode).

882 K. Uluc et al. / Clinical Neurophysiology 119 (2008) 880–885

that provided a supramaximal nerve action potential with-out a muscle twitch, we recorded the potential. To test dor-sal sural NAP, the recording electrode was placed along aline from the stimulating site to the fifth toe over the lateralaspect of the foot. The stimulation site was posterior to thelateral malleolus, with the cathode placed 100 mm proxi-mal from the recording electrode. A ground electrodewas placed on the dorsum of the foot equidistant betweenthe recording and the stimulating electrodes (Oh, 2003)(Fig. 2).

2.3. Statistical analysis

Statistical analyses were performed on NCS data thatwere obtained from the subjects. Normal distribution ofNCS parameters were tested by Shapiro–Wilk normalitytest. Clinical measures were compared using the chi-squareor Fisher exact tests for proportions. To compare the groupmeans Mann–Whitney U test was used and Pearson’s corre-lation coefficients were utilized for correlation analysis. A P

value < 0.05 was considered significant. The upper or lowerlimits of normal values for NCS were obtained from the con-trol group by calculating mean ± 2 standard deviations(SD). The values not within this range were considered asabnormal.

Fig. 2. Dorsal sural nerve conduction technique and a dorsal sural SNAPelectrode; G, ground electrode).

3. Results

3.1. Clinical findings

The mean ± SD age of patients was 52.7 ± 6.1 years(range 38–59 years), while the mean ± SD age of the con-trol group was 49.7 ± 6.6 (range 33–59 years) and therewas no significant age difference between groups(P = 0.08). In addition, the normal and diabetic groupsmatched in height. One patient had type 1 DM, and allthe other patients had type 2 DM. Mean duration of theDM was 91.3 months (range 1–324 months). Eleven ofthe patients were taking insulin and 19 of them were takingoral antidiabetic drugs. The mean duration of neuropathicsymptoms at the time of evaluation was 27.8 ± 36 months(range 1–120 months). All patients complained of symmet-rical painful dysesthesias including burning or lighteningpains and numbness in the feet and lower legs. Amongthe patients, three (10%) had hyperalgesia, while none ofthem described allodynia. On neurological examination,24 (80%) patients had reduced pinprick sensitivity and tem-perature loss. Vibration sensation was abnormal in 17(56%) patients, and four (13%) patients had abnormal pro-prioception. Muscle stretch reflexes at the ankles werereduced in 13 (43%), and absent in two (7%) patients. None

recording from a control subject (S, stimulating electrode; R, recording

Table 1Results of medial plantar and dorsal sural nerve conduction studies incontrols and diabetic patients

Controls(N = 30)

Diabetics(N = 30)

Pa

K. Uluc et al. / Clinical Neurophysiology 119 (2008) 880–885 883

of the patients were classified in the LFN group. While 18(60%) patients had clinically MFN, 12 (40%) of the 30patients were classified in the SFN group. Age and genderdid not differ between MFN and SFN patients. Themean ± SD of NIS (LL) was 5.27 ± 2.9.

Medial plantar nerve

Amplitude (lV)Mean ± SD 9.4 ± 4.2 3.1 ± 2.8 0.005a

Maximum 21.6 8.6Minimum 4.6 0Number of noresponse

0 9

Onset NCV (m/s)b

Mean ± SD 57 ± 8.1 53.6 ± 8.9 0.15Maximum 75 70.3Minimum 42.1 36.2

Peak NCV (m/s)b

Mean ± SD 43.3 ± 5 42.7 ± 6.3 0.52Maximum 51 54.5Minimum 32.4 29.3

Dorsal sural nerve

Amplitude (lV)Mean ± SD 7.9 ± 3.3 3.3 ± 3.5 0.004a

Maximum 17.9 12.6Minimum 3.5 0Number of noresponse

0 11

Onset NCV (m/s)b

Mean ± SD 44.6 ± 5.2 41.6 ± 7.3 0.038a

Maximum 56.5 64.3Minimum 44.6 34.4

Peak NCV (m/s)b

Mean ± SD 34.5 ± 4.2 32.3 ± 4.4 0.13Maximum 43.3 40.9Minimum 34.4 26.7

SNAP, sensory nerve action potential; SD, standard deviation; NCV,nerve conduction velocity.

a Significant value.b In subjects with obtainable nerve action potential.

3.2. Electrophysiological findings

In all control subjects, we obtained nerve action poten-tials of the medial plantar and dorsal sural nerves. In thecontrol group, the mean onset and mean peak latenciesof the dorsal sural nerve were 2.3 ± 0.3 ms (range 1.9–3.25 ms) and 3.0 ± 0.4 ms (range 2.4–4.1 ms), respectively.The mean maximum and mean negative-peak NCVs were44.6 ± 5.2 m/s (range 34.4–56.5 m/s) and 34.5 ± 4.2 m/s(range 26.7–43.3 m/s). Mean NAP amplitude of the dorsalsural was 7.9 ± 3.3 lV. These results were comparable toOh’s findings (Oh, 2003). For the medial plantar nerve,mean amplitude of the control group was 9.4 ± 4.2. AsShapiro–Wilk normality test showed that NAP amplitudesof the dorsal sural and medial plantar nerves were not nor-mally distributed, lower limits of normal values for thesenerves were calculated as mean � 2 SD of logarithmictransformed data. The lower limits of normal (inversed log-arithmic value) of the dorsal sural and medial plantaramplitudes were 3.1V and 4.1 lV, respectively. On theother hand, mean amplitudes of the dorsal sural and med-ial plantar nerves in the patients were 3.3 ± 3.5 and3.1 ± 2.8 lV, respectively (P = 0.004 for dorsal sural,P = 0.005 for medial plantar).

As NAP of the medial plantar and dorsal sural nervescould not be obtained bilaterally in some patients, theirNCVs could not be calculated. So, in those patients, weonly used amplitude values of the medial plantar and dor-sal sural nerves in the statistical analysis. On the otherhand, in subjects with obtainable NAP, no significant dif-ference was found between patients and healthy subjectsfor the mean onset and mean peak NCV of the medialplantar nerve and for the peak NCV of the dorsal suralnerves (P > 0.05). However, the onset NCV of the dorsalsural nerve was significantly slower in patients than con-trols (P = 0.038). The detailed results of the medial plantarand dorsal sural NCS in the control and patient groups arelisted in Table 1.

Nine patients had electrophysiologically diagnosed car-pal tunnel syndrome. Otherwise, in routine NCS, no signif-icant difference was found between clinically defined DSNpatients and control subjects that were done in the upperextremity. For the routine NCS that were performed inthe lower extremities, although there were significant differ-ences between group means for F-latencies of the tibial andperoneal nerves in the patient and control groups (P = 0.01for tibial, P = 0.00 for peroneal), none of the patients hadabnormal result for the F-latency of the peroneal nerve(>54.4 ms) and only two patients had abnormality for tib-ial nerve (>55.7 ms). Mean minimum F-latency of the pero-

neal nerve was significantly prolonged in patients withMFN than patients with SFN (P = 0.01).

In all patients, NAP amplitudes of the sural and superfi-cial peroneal nerves were within normal ranges, but in thepatient group mean value was significantly lower than thecontrol group (P = 0.04). The mean ± SD amplitude ofthe sural nerve was 11.7 ± 4.6 lV for the patient groupand 16.8 ± 6.1 lV for controls. The mean ± SD amplitudeof the superficial peroneal nerve was 7.8 ± 2.7 lV forpatients and 10.5 ± 3.8 lV for controls. The lower limitsof normal (inversed logarithmic value) of the sural andsuperficial peroneal nerve amplitudes were 7.4 and 4.6 lV,respectively. For peak NCV of the superficial peronealand sural nerves and for onset NCV of the sural nerves,there were significant differences between patients andhealthy subjects (P = 0.009, 0.001 and 0.007, respectively).However, none of the patients had abnormal values (i.e.below the lower limits of normal) for peak NCV of the supe-rior peroneal and sural nerves, and only one patient hadabnormality for onset NCV of the sural nerve.

Table 2Sensitivity and specificity of bilateral assessment of medial plantar, dorsalsural and medial plantar plus dorsal sural nerves

Abnormal NCS(patients)

Sensitivity(%)

Medial plantar nerve 18 60Dorsal sural nerve 13 40Medial plantar + dorsal sural nerve 21 70

884 K. Uluc et al. / Clinical Neurophysiology 119 (2008) 880–885

Among clinically defined 30 DSN patients, medial plan-tar NAP amplitude was abnormal in 18 (60%) patientsbilaterally. On the other hand, 13 (40%) of the patientshad bilaterally abnormal dorsal sural NAPs. Accordingto these results, calculated sensitivity of NAP amplitudeof the medial plantar and dorsal sural nerves in our studyis shown in Table 2. Both mean medial plantar and dorsalsural NAP amplitudes were lower in patients with MFNand SFN than control subjects (P = 0.00 for medial plan-tar, P = 0.00 for dorsal sural in MFN group; P = 0.00for medial plantar, P = 0.01 for dorsal sural in SFNgroup). On the other hand, although patients with MFNhad a tendency to have lower medial plantar NAP ampli-tudes than the SFN patients, the difference was not signif-icant (P = 0.07).

In the patient group, we did not find any significant cor-relation between duration of the DM and neuropathicsymptoms and NAP amplitude of sural, dorsal sural andmedial plantar nerves. In patients, NIS (LL) scores weresignificantly correlated with NAP amplitude of the medialplantar nerve (P = 0.02), but not with NAP amplitudes ofthe sural and dorsal sural nerves. In all patients who hadabnormal position sensation and hypoactive ankle reflexesin the MFN group, NAP amplitude of the medial plantarnerves was also abnormal.

4. Discussion

The main aim of this study was to investigate the clinicalutility of medial plantar and dorsal sural NCS in the detec-tion of polyneuropathy. We have studied a population ofdiabetics with clinical signs and symptoms of polyneurop-athy and compared them with healthy controls. We foundthat both medial plantar and dorsal sural NAPs could reli-ably be recorded in healthy subjects under the 60 years ofage. But, in patients with clinically defined polyneuropathyNAP amplitudes of these nerves were significantly abnor-mal compared to the sural nerve and superficial peronealnerves. Additionally, mean onset NCV of the dorsal suralnerve was significantly slower in DSN patients than inthe control group.

Dorsal sural NCS were first performed by Burke et al.(1974). Later on, in a study of standardization of distalsural nerve conduction in 40 healthy adult subjects,responses from dorsal sural nerve were obtained from allsubjects, and it was suggested that electrodiagnostic evalu-ation of the distal sural nerve could be readily achieved(Lee et al., 1992). In Killian and Foreman’s study, NAP

of the dorsal sural nerves was bilaterally found absent in97% of the patients with peripheral neuropathies with dif-ferent etiologies (Killian and Foreman, 2001). In thatstudy, sural nerve NAP was absent in 70% of those patientsand by evaluating the dorsal sural NCS, the investigatorsdiagnosed neuropathy in 16 patients who had been evalu-ated as normal due to their normal sural NAPs. Comparedto Killian and Foreman’s study, we found a lower rate ofabnormality in dorsal sural NCS; one explanation for thisfinding might be the more advanced stage of neuropathyand large-myelinated fiber involvement in their patients.In addition, in their series all patients had clinical andapproximately half of the patients had electrophysiologicalinvolvement of motor nerves. In a preliminary study, Ala-pati et al. found abnormalities in the nerve conduction ofthe dorsal sural NCS in 20–25% of DSN cases with normalroutine NCS in comparison to 60% of cases by the near-nerve needle interdigital nerve conduction (Alapati et al.,2004). The clinical utility of dorsal sural NCS in diabeticchildren and adult patients were shown in two consecutivepapers sent from the same medical center (Turgut et al.,2004; Balci et al., 2005). Turgut et al. found longer latencyand slow conduction velocity in the dorsal sural nerve indiabetic children who had no sensory sign or symptom ofperipheral neuropathy. By using dorsal sural NCS, Balciet al. revealed low SNAP amplitude in adult diabeticpatients with clinical symptoms and signs of neuropathy(Balci et al., 2005). Thus, all these studies clearly showedthe reliability and higher diagnostic sensitivity of the dorsalsural NCS over routine NCS.

Medial plantar NCS with surface electrodes generally arather favored method than dorsal sural NCS in the diag-nosis of polyneuropathy (Løseth et al., 2007; Herrmannet al., 2004; Nodera et al., 2002). Nodera et al. (2002) car-ried out sural and medial plantar NCS in 133 patients withDSN. They found that the sensitivity of detection of neu-ropathy was increased from 27% to 69% by using the med-ial plantar NCS instead of NCS of the sural nerve. Inanother study, assessing the medial plantar SNAP and skinbiopsy in the evaluation of suspected DSN, Herrmannet al. (2004) found abnormality in medial plantar SNAPin 20.4% of patients with small fiber neuropathy and42.9% of patients with sensory neuropathy with large-mye-linated fiber involvement. They concluded that the medialplantar SNAP and skin biopsy were complimentary inevaluation of DSN. In a recently published paper, Løsethet al. (2007) also showed the reliability of the medial plan-tar nerve response in patients with DM less than 70 years.Their findings were similar to the findings of Nodera’sstudy. While, they found abnormal medial plantar NCSin 59% of patients, sural NCS were abnormal only in24% of patients. In agreement with the studies mentionedabove, we observed that medial plantar response was themost frequently abnormal one compared to sensory nervesthat are tested in routine NCS. We thought that this find-ing is related with the dying back phenomenon of DSN.Compared to sural NCS, assessment of medial plantar

K. Uluc et al. / Clinical Neurophysiology 119 (2008) 880–885 885

NCS we carried out amplified the sensitivity to 60% in thedetection of neuropathy. Additionally, performing bothmedial plantar and dorsal sural NCS increased the sensitiv-ity to 70% in diabetic patients who had been considered asnormal according to routine NCS. Very recently, Hemmiet al. (2007) described a new technique that evaluates themore distal portions of the medial plantar nerves. With thissimple method, they could obtain medial plantar SNAPs in63 of 64 of the control subjects. In addition, although theyperformed it in a very few patients with clinically defineddiabetic polyneuropathy, the investigators found themethod sensitive in the early diagnosis of sensoryneuropathy.

Although NCV and F-latency variables were signifi-cantly different in patient and control groups, they wereinsufficient individually in defining abnormality of patients.Detection of abnormalities on patient base is more valu-able than group means and assessment of medial plantarand dorsal sural nerve NAP amplitudes were sufficientnot only in discriminating patient group from healthy sub-jects but also revealing in the abnormality on individualbase. We think that, the later discrimination could be moreuseful in clinical practice.

Even though, sural or superficial nerves are usuallyaffected in diabetic polyneuropathy (Nodera et al., 2002;Løseth et al., 2007), we obtained sural and superficial NAPsin all patients, and they were in normal ranges. On the basisof the clinical and electrophysiological data, one explanationof this finding might be the study population was not biasedtoward individuals with severe polyneuropathy and involveda small group of patients with slight diabetes.

In our study, we found lower NIS (LL) scores in thepatients than the study of Løseth et al. and correlationbetween the NIS (LL) and electrophysiological findingswas not in harmony with that study. Løseth et al. foundthat the mean NIS (LL) of those with abnormal NCSwas highest when the more proximal nerves (sural andsuperficial peroneal) were involved (Løseth et al., 2007).On the other hand, we only found a significant correlationbetween NIS (LL) scores and medial plantar SNAP. Thereason for no correlation between sural SNAPs and NIS(LL) in our study could be explained by the small samplesize.

Unilateral abnormality of the medial plantar and dorsalsural nerves does not necessarily indicate the presence ofDSN. Although rare, this can be due to damage or entrap-ment of these nerves. SNAPs should be bilaterally absentto diagnose DSN. In all patients with neuropathy who par-ticipated in this study, the medial plantar and dorsal suralwere abnormal bilaterally.

In summary, bilateral assessment of NCS of both ofthese nerves is a highly sensitive method for detecting

DSN. These tests are easily performed in the clinical settingwith surface electrodes and with standard equipment andthey are non-invasive. We suggest that neurophysiologicalexamination of both medial plantar and dorsal sural nervesdecreases the risk of underrecognition of DSN comparedto use of either nerve alone and should be included in com-plete workup of patients with neuropathic symptoms.

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