Sural Sensory Nerve Action Potential Amplitude Research Articles

Age-Related Changes in Neurologic Examination and Sensory Nerve Amplitude in the General Population: Aging of the Peripheral Nervous System.

Chronic axonal polyneuropathy is a common disease of the peripheral nervous system with increasing prevalence with age. Typical neurologic signs are present in patients with polyneuropathy but may also occur in individuals without disease. Owing to limited knowledge on normal aging of the peripheral nervous system, it can be difficult to distinguish peripheral nerve dysfunction due to disease from variations in normal aging. Therefore, we described the changes in neurologic examination and nerve conduction studies that accompany aging in the general population. In this cross-sectional population-based study, we screened participants for chronic polyneuropathy in a controlled environment using standardized methods including a symptom questionnaire, neurologic examination, and nerve conduction studies (NCS). Inclusion criteria were 40 years or older and living in a suburb of Rotterdam, the Netherlands. Participants not diagnosed with chronic polyneuropathy, based on the discussion of findings in the screening by an expert team, were included to determine the effect of age (range 41-96 years) on features of neurologic examination and NCS using frequency calculations and quantile regression analysis. In total, 4,179 participants (mean age 64.5 ± 12.7 years, 54.9% female) were included of whom 3,780 (90.5%) did not fulfil the criteria for polyneuropathy. In the population without polyneuropathy, the frequency of normal features at neurologic examination declined with age, most pronounced for vibration sense at the hallux (from 6.6 [SD ± 1.5] in 40-49 years to 3.6 [SD ± 3.1] in 80 years or older) and Achilles tendon reflexes (absent in 9% in 40-49 years up to 33% in 80 years or older). Superficial pain sensation and patellar tendon reflexes remained stable over time. Sural sensory nerve action potential (SNAP) amplitude declined with age from 11.2 μV in 40-49 years to 3.3 μV in 80 years or older. Nonrecordable SNAP amplitudes were found in 25.1% of the participants older than 80 years, more often in men (30.3%) than in women (21.0%). This study showed the effect of age on features of neurologic examination and sural nerve amplitude in the general population. These findings are helpful to distinguish features suggesting polyneuropathy from variations of normal aging of the peripheral nervous system.

Age-related sensory neuropathy in patients with spinal muscular atrophy type 1.

Spinal muscular atrophy type 1 (SMA 1) is a devastating motor neuron disorder that leads to progressive muscle weakness, respiratory failure and premature death. Although sensory electrophysiological changes have been anecdotally found in pediatric SMA 1 patients, the age of onset of sensory neuropathy remains unknown. Sensory nerve conduction studies of the median and sural nerves were performed in 28 consecutive SMA 1 patients of different ages. Sensory nerve conduction velocities and sensory nerve action potential (SNAP) amplitudes recorded in these patients were compared with those obtained from 93 healthy subjects stratified by age. SNAP amplitudes decreased with increasing age in the sural and median nerves, without any significant difference between upper and lower limbs. Our data suggest that sural and median nerve SNAP amplitudes are normal in younger patients, while an axonal neuropathy appears in older ones.

The relationship between nerve conduction studies and neuropathic pain in sciatic nerve injury due to intramuscular injection.

BackgroundSciatic nerve injury due to intramuscular injection (SNIII) is still a health problem. This study aimed to determine whether there is a correlation between neuropathic pain and electrodiagnostic findings in SNIII.MethodsPatients whose clinical and electrodiagnostic findings were compatible with SNIII participated in this retrospective cohort study. Compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes of the sural, superficial peroneal, peroneal, and tibial nerves were graded from 1 to 4. Leeds assessment of neuropathic symptoms and signs scale (LANSS) was applied to all patients.ResultsForty-eight patients were included in the study, 67% of whom had a LANSS score ≥ 12. Sural SNAP amplitude abnormalities were present in 8 (50%) out of 16 patients with a LANSS score < 12, and 28 (87.5%) out of 32 patients with a LANSS score ≥ 12, with significant differences between the groups (P = 0.011). There was a positive correlation between the LANSS score and the sural SNAP amplitude grading (P = 0.001, r = 0.476). A similar positive correlation was also found in the LANSS score and the tibial nerve CMAP amplitude grading (P = 0.004, r = 0.410).ConclusionsThis study showed a positive correlation between the severity of tibial nerve CMAP/sural SNAP amplitude abnormality and LANSS score in SNIII. Neuropathic pain may be more common in SNIII patients with sural nerve SNAP amplitude abnormality.

Diet quality and chronic axonal polyneuropathy: a population‐based study

ObjectiveTo investigate the association between diet quality and chronic axonal polyneuropathy.MethodsBetween June 2013 and January 2017, among 1650 participants of the Rotterdam Study (median age 69.1 years, 54.2% women), diet quality was quantified based on food frequency questionnaires as a sum score of adherence (yes/no) to 14 components of the Dutch dietary guidelines. Presence of polyneuropathy was determined based on a questionnaire, neurological examination of the legs, and nerve conduction studies. We used logistic regression to associate diet quality with the presence of chronic axonal polyneuropathy and linear regression to associate with sural sensory nerve action potential (SNAP) amplitude in participants without polyneuropathy. Results were adjusted for age, sex, time between measurements, body mass index, blood pressure, diabetes mellitus, smoking, kidney function, and education.ResultsOverall diet quality was not associated with chronic axonal polyneuropathy (odds ratio [OR] = 0.99, 95% confidence interval [CI] 0.88; 1.12, P = 0.842), nor with sural SNAP amplitude in participants without polyneuropathy (difference = 0.01, 95% CI −0.14; 0.15, P = 0.993). Although not surviving multiple testing, a nominally significant association was found between salt intake ≤6 g/day and presence of chronic axonal polyneuropathy (OR = 0.55, 95% CI 0.35; 0.86, P = 0.008).InterpretationWe did not find an association between diet quality and chronic axonal polyneuropathy.

Sural nerve sensory response in diabetic distal symmetrical polyneuropathy.

The sural sensory nerve action potential (SNAP) amplitude is a measure of the number of axons. We tested the hypothesis that sural SNAP amplitude can be used as a marker in screening, severity evaluation, and follow-up of diabetic distal symmetrical polyneuropathy (DSPN). Patients with type 2 diabetes underwent nerve conduction studies and were followed for 6 years. Composite amplitude scores (CASs) were determined to evaluate DSPN severity. Sural SNAP amplitudes were negatively correlated with CAS (r = -.790, P < .0001), and changes in sural SNAP amplitudes were negatively correlated with those of CAS after controlling for follow-up duration (r = -.531, P = .028). When a patient's baseline sural SNAP amplitude is above zero, it can be used as one measure of DSPN in screening, severity evaluation, and follow-up. However, if the patient's sural SNAP value is zero, CAS can be used as a follow-up measure.

F31. Longitudinal neurophysiological study of dominant intermediate Charcot-Marie-Tooth type C neuropathy

Dominant intermediate Charcot-Marie-Tooth neuropathy subtype C (DI-CMTC) is associated with mutations in the YARS gene, encoding tyrosyl-tRNA synthetase (TyrRS). In a prospectively designed study we were the first to report the phenotype and genotype of DI-CMTC from a U.S. and a Bulgarian family using electrodiagnostic (EDX) and morphological studies. Here we present longitudinal data for the U.S. family 16 years after the initial evaluation. After re-consenting, 13 of 21 original DI-CMTC participants underwent EDX and physical examinations. Data of 2000 and 2016 were compared for specific nerves using paired t-tests. General linear model univariate analysis was used to relate findings to patient age. Data are presented as mean ± SD. Four women and 9 men were examined at ages 8–77 years in 2000 and 24–93 years in 2016. During this time median nerve compound muscle action potential (CMAP) amplitudes decreased from 9.3 ± 2.9 mV to 6.0 ± 2.9 mV (p = 0.002), while distal motor latencies (DML) increased from 4.2 ± 0.6 ms to 4.5 ± 0.6 ms (p = 0.04); mean motor nerve conduction velocity (MNCV) remained largely unchanged at 37 m/s. Over the same period ulnar nerve CMAP amplitudes decreased from 9.2 ± 2.1 mV to 6.1 ± 1.8 mV (p = 0.004); mean MNCV remained the same at 39 m/s. In 2000 and 2016 all adult participants had absent peroneal motor responses, as well as absent tibial responses (except for 2 patients with CMAP amplitudes <1 mV and MNCV 32–35 m/s in 2000 and 28–32 m/s in 2016). In the interval sural sensory nerve action potential (SNAP) amplitudes changed from 2.0 ± 2.5 mV to 1.0 ± 2.4 mV (p = 0.10), and sensory nerve conduction velocities (SNCV) from 39.3 ± 1.0 to 35.5 ± 2.1 m/s (p = 0.13); this did not reach statistical significance. Median nerve sensory peak latencies increased from 3.4 ± 0.4 to 3.9 ± 0.4 ms (p = 0.01), SNAP amplitudes changed from 7.2 ± 5.3 to 6.5 ± 5.1 mV (p = 0.055), and SNCV from 46 ± 1.7 to 41.3 ± 7.6 m/s (p = 0.328). There was an age-dependent decrease of CMAP amplitudes of median (p = 0.044), peroneal and tibial (p < 0.001), and SNAP amplitudes of median(p = 0.008), radial (p = 0.013) and sural (p = 0.028). EMG revealed distal dominant acute and chronic denervation and reinnervation in lower limb muscles and some hand muscles. In this study MNCV remained stable over 16 years, but motor and sensory amplitudes decreased. DI-CMT C appears to produce a progressive age- and nerve length-dependent axonal degenerative process. Longitudinal EDX findings are consistent with our previous cross-sectional morphological study of sural nerves, which also revealed an age-dependent loss of large and small myelinated axons.

Role of "Sural Sparing" Pattern (Absent/Abnormal Median and Ulnar with Present Sural SNAP) Compared to Absent/Abnormal Median or Ulnar with Normal Sural SNAP in Acute Inflammatory Demyelinating Polyneuropathy.

Sural sparing defined as absent/abnormal median sensory nerve action potential (SNAP) amplitude or absent/abnormal ulnar SNAP amplitude with a normal sural SNAP amplitude is thought to be a marker for inflammatory demyelinating polyneuropathies. If sural sparing pattern specifically defined as absent/abnormal median and ulnar SNAP amplitude with normal sural SNAP amplitude (AMUNS) is sensitive and specific when compared with either absent/abnormal median and normal sural (AMNS) or absent/abnormal ulnar and normal sural (AUNS) for acute inflammatory demyelinating polyneuropathy (AIDP), chronic inflammatory demyelinating polyneuropathy (CIDP), select non-diabetic axonopathies (AXPs), and diabetic neuropathies (DNs). Retrospective analysis from 2001 to 2010 on all newly diagnosed AIDP, CIDP, select non-diabetic AXP, and DN. There were 20 AIDP and 23 CIDP. Twenty AXP and 50 DN patients between 2009 and 2010 were included as controls. AMUNS was seen in 65% of AIDP, 39% CIDP compared with 10% of AXP and 6% for DN with sensitivity of 51%, specificity of 92%, whereas the specificity of AMNS/AUNS was 73% and its sensitivity was 58%. If a patient has AMUNS they are >12 times more likely to have AIDP (p < 0.001). Sural sparing is highly specific but not sensitive when compared with either AMNS or AUNS in AIDP but does not add to sensitivity or specificity in CIDP.

High body mass and kidney dysfunction relate to worse nerve function, even in adults without neuropathy.

Polyneuropathy is a prevalent and disabling disorder. Despite extensive evaluation, the cause often remains unknown. Factors that predispose for the development of polyneuropathy need to be identified. We investigated the effect of anthropometric and metabolic factors on peripheral nerve function in 908 participants of the population-based Rotterdam Study without any symptoms or signs of polyneuropathy. Participants underwent nerve conduction studies of the sural and peroneal nerve. Data on age, height, weight, waist circumference, diabetes, lipid levels, hypertension, and kidney function were collected. Regression analyses were used to investigate determinants of nerve action potential amplitudes. The frequency of abnormal sural sensory nerve action potential (SNAP) amplitudes increased with age from 1% under 60 years to 23% over 80 years. Similarly, the frequency of abnormal peroneal nerve compound motor action potential (CMAP) amplitudes increased from 4% to 13%. High weight and body mass index were independently associated with reduced sural SNAP amplitudes and peroneal CMAP amplitudes. Participants with hypertension and kidney dysfunction were more likely to have abnormal sural SNAP amplitudes. Older age, high weight, hypertension, and moderate kidney dysfunction might thus lead to peripheral nerve dysfunction in persons yet without symptoms or signs of polyneuropathy.

Dorsal Sural Sensory Nerve Action Potential: A Study for Reference Values.

Background:Dorsal sural sensory nerve action potential (SNAP) could help diagnose early or subclinical peripheral neuropathy.Objectives:To establish reference data for dorsal sural SNAP amplitude, latency, and velocity in healthy participants.Materials and Methods:A prospective study was conducted in 45 nerves from healthy participants between 18 and 90 years and stratified into three age groups (a = 18–40 years, b = 41–60 years, and c>60 years). StataCorp 12.2 statistical program was used for all statistical analyses. Mean-2 standard deviation was used to generate reference values for the lower limit of amplitude and velocity in each age group. ANOVA with Bonferroni correction was used for intergroup comparisons of amplitude and velocity. Regression analysis was used to compute an equation for the predicted amplitude with age, height, and weight as the covariates.Results:The lower limit for amplitude (uv) in Groups a, b, and c was 2.57, 1.97, and 1.01, respectively. The lower limit for velocity (m/s) was 33.6, 32, and 22.8, respectively. Statistical significance was noted between the amplitudes of participants in Groups b and c (P = 0.039) and a and c (P = 0.001). Similarly, velocity was significantly different between Groups b and c (P = 0.04) and a and c (P = 0.008). Age was the covariate with maximum effect on the dorsal sural amplitude. Gender and side-to-side comparison did not show statistical significance for amplitude and velocity measurements. Linear regression analysis of the transformed amplitude gave the predictive equation as (y) =3.338 + age (−0.0167) + height in meters (−0.209) + weight (0.001).Conclusion:This study provides reference data for dorsal sural SNAP in Indian population stratified by age.

The diagnostic accuracy of Sudoscan in transthyretin familial amyloid polyneuropathy.

Transthyretin familial amyloid polyneuropathy (TTR-FAP) is an axonal sensory-motor and autonomic neuropathy. Reliable quantification of sudomotor function could prove essential in the diagnosis and early treatment management. We aim to assess the diagnostic value of a new sudomotor test (Sudoscan) in TTR-FAP. One hundred and thirty-three TTR-FAP Val30Met carriers, divided in asymptomatic and symptomatic stage 1, were compared with 37 healthy controls. We analyzed the right sural sensory nerve action potential (SNAP), the plantar sympathetic skin response (SSR) and the electrochemical skin conductance (ESC) measured by Sudoscan in both hands and feet. All neurophysiological measures were significantly worse in the symptomatic group. However, feet ESC was the only test distinguishing symptomatic patients with autonomic dysfunction from those without autonomic dysfunction, and both groups from asymptomatic subjects and healthy controls. Feet ESC was a significant independent predictor for the presence of symptoms and autonomic failure, after adjusting for demographic characteristics, sural SNAP and SSR amplitudes (p<0.05). Feet ESC showed 76% sensitivity and 85% specificity for detection of dysautonomia. Feet ESC is a sensitive test to assess early autonomic dysfunction in TTR-FAP subjects. This investigation should be considered for routine assessment in this population. Abnormal feet responses on Sudoscan support early diagnosis in TTR-FAP.

Sensory changes in pediatric patients with spinal muscular atrophy: an electrophysiologic study

Spinal muscular atrophy (SMA) is well known to be a pure motor neuron disease. However, it was reported that sensory neuron degeneration can also occur in pediatric SMA. The aim of the present study was to assess peripheral and central sensory abnormalities in pediatric SMA patients. The present study included 29 type I and 11 type II SMA patients diagnosed on the basis of clinical history and typical electromyographic patterns, and 25 age-matched and sex-matched healthy pediatric participants, who comprised the control group. Sensory and motor conduction studies were carried out for both groups. Sensory conduction studies of sural and median nerves assessed peak latency, sensory nerve action potential (SNAP) amplitude, and sensory nerve conduction velocity. Mixed posterior tibial somatosensory evoked potential latency and amplitude were also assessed for both groups. SMA I patients had lower sural and median SNAP amplitudes, as well as lower peroneal and femoral compound muscle action potential amplitudes, slower tibial motor conduction velocity (MCV), and prolonged femoral and peroneal distal latency compared with the control group. SMA II patients had lower sural SNAP amplitude, slower sural sensory nerve conduction velocity, lower tibial somatosensory evoked potential amplitude, and lower tibial peroneal and femoral compound muscle action potential amplitudes, as well as slower tibial motor conduction velocity and prolonged peroneal distal latency, compared with the control group. Sensory neuron and/or axonal affection have been demonstrated in the studied series of pediatric SMA patients suggesting that the pathological changes in SMA may also involve the sensory system.

Sural and Radial Sensory Responses in Patients with Sensory Polyneuropathy.

The sural/radial nerve amplitude ratio (SRAR) is the quotient of the sensory nerve action potential (SNAP) amplitudes (Amp) of the sural and the superficial radial nerve. It has been hypothesized that this ratio can be used for the detection of early axonal loss, because the sural SNAP amplitude will decrease first, thereby also decreasing the SRAR value. To determine the sensitivity and specificity of SRAR, age-adjusted sural and radial SNAP Amp in the diagnosis of axonal sensory polyneuropathy in cancer patients. Retrospective review. Comprehensive cancer center. One hundred and ninety one EMG reports from January 2001 to December 2005. The independent variable is the diagnosis of axonal sensory polyneuropathy in the EMG reports that is based on multiple tests. We assessed the agreement between classifications of axonal sensory polyneuropathy made using the current 'gold standard' and the proposed method that is based on patients' age-adjusted radial and sural SNAP amplitude; an SRAR being above or below the normal value (0.21). We found that the sensitivities for age-adjusted radial SNAP Amp, age-adjusted sural SNAP Amp, and SRAR were 33%, 64%, 56% respectively; the specificities were 85%, 70%, 77% respectively. SRAR is neither the most sensitive, nor the most specific in the diagnosis of axonal sensory polyneuropathy.

Cardiovagal and somatic sensory nerve functions in healthy subjects.

Heart rate response to deep breathing (HRDB), which depends on the integrity of cardiac vagal preganglionic neurons and efferent fibers, and the function of sural nerve fibers are both associated with an age-related decline process. The aim of this study was to determine whether the effects attributed to aging on cardiovagal and sural nerve function decline are associated. HRDB and sural sensory nerve action potential (SNAP) amplitude, latency, and conduction velocity (SCV) were measured in one hundred healthy asymptomatic subjects (aged 14-92 years, 41 women). Multiple and simple linear regressions were used to analyze the relationships between the variables. There were significant linear relationships between sural SNAP amplitude and HRDB with age. There was also a significant linear relationship between sural SNAP amplitude and HRDB (correlation coefficient 0.46, p<0.0001), but the model explained only 21.5% of the variability in HRDB. Cardiovagal function assessed by HRDB is associated with sural SNAP amplitude in healthy subjects. Age-related decline only partially explained the variability seen in the association. Other genetic and environmental factors may also play a role.

Effect of coexistent carpal tunnel abnormality on sensory conduction findings in polyneuropathy.

To investigate the change of pattern of sensory conduction findings in polyneuropathy with coexistent carpal tunnel abnormality (CTAbN). We reviewed sensory conduction findings of 46 patients with acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and 66 with diabetic polyneuropathy (DP). Both groups were categorized into those with and without CTAbN according to transcarpal median sensory conduction velocities. In AIDP, median sensory nerve action potential (SNAP) amplitudes were reduced, whereas sural SNAP amplitudes remained unchanged. Median SNAP amplitude was lowest, and sural/median SNAP amplitude ratio was highest in AIDP with coexistent CTAbN. In DP, both median and sural SNAP amplitudes were reduced. Their sural/median SNAP amplitude ratios remained unchanged. Incidence of abnormal median-normal sural pattern was higher in AIDP than in DP. Nevertheless, these incidences did not alter with coexistent CTAbN. The ulnar SNAP amplitude and sural/ulnar SNAP amplitude ratio were not significantly different between those with and without CTAbN in both AIDP and DP groups. Coexistent CTAbN caused further increase of sural/median SNAP amplitude ratio only in AIDP.

Misinterpretation of sural nerve conduction studies due to anatomical variation

ObjectiveAnatomical variation of the sural nerve has been documented in numerous cadaver studies. The sural nerve conduction parameters can potentially be influenced by the sural nerve type A formation formed by the union of the medial sural cutaneous nerve (MSCN) and the peroneal communicating branch (PCB) and the type C formation with the sural nerve formed solely by the PCB. MethodsIn 17 out of 240 prospectively examined subjects referred for polyneuropathy a suspicion of an anatomical variation of the sural nerve was raised due to decreased amplitude or substantial side-to-side variation (>50%) of the sensory nerve action potential (SNAP) in disproportion to the clinical findings. To verify the variation the sural nerve was examined further with surface electrodes and near-nerve technique, including extra lateral and distal needle placements. ResultsIn all 17 subjects an anatomical variation affecting the sural SNAP was confirmed as a normal sural SNAP could be obtained by changing the electrode placement. The most frequent variation, seen in 15 subjects, was a type A formation with union of the MSCN and the PCB distally at low calf, while a type C formation was seen in 2 subjects. ConclusionsIn case of a decreased sural SNAP amplitude or substantial side-to-side variation in disproportion to the neurologic evaluation, an anatomical variation instead of pathology could be suspected and a different electrode placement be considered. SignificanceNeurophysiologists should be aware of different types of formations of the sural nerve which may cause misinterpretations of nerve conduction studies, especially when needle electrodes are used.

Sensory Conduction Study in Fisher Syndrome: Patterns of Abnormalities and Their Clinical Correlation

Objective: To report sensory conduction findings in patients with typical Fisher syndrome (FS) and to determine if a specific pattern of sensory conduction abnormalities was present in such patients. Methods: We retrospectively reviewed results of sensory conduction studies of 55 FS patients and compared them with those obtained from 83 age- and sex-matched healthy volunteers. Results: Mean median and ulnar sensory nerve action potential (SNAP) amplitudes were lower in FS patients than in normal subjects, whereas sural SNAP amplitudes were not different between the two groups. Abnormal median/ulnar sensory responses (reduced SNAP amplitude or absent response) were more frequently observed than abnormal sural response. Normal sensory conduction results were found in 31 (56%) patients. Of the 24 (44%) patients with abnormal sensory findings, 18 (33%) had a sural-sparing pattern of abnormalities. Patients with impaired sensation had lower median and ulnar SNAP amplitudes than those without. Conclusions: Abnormal median and ulnar sensory responses were the most frequent sensory findings in FS. Findings of the sural-sparing pattern of abnormalities suggest distal sensory nerve involvement in these patients.

Neurophysiological examination of dorsal sural nerve

Nerve conduction study of the dorsal sural nerve (DSN) has been reported to be a sensitive method for early detection of peripheral neuropathies. However, normal reference values are scarce and vary greatly among the different studies. A comprehensive neurophysiological study, including nerve conduction velocity (NCV) and sensory nerve action potential (SNAP) recording, was performed in 294 healthy subjects (21-86 years) with no evidence of neuropathy. The amplitude of the DSN SNAP ranged from 2.50 to 15.90 μV, and NCV ranged from 28.9 to 52.8 m/s. A significant age-related decrease in DSN SNAP amplitude and NCV was observed. The mean ratio of sural NCV to DSN NCV was 1.33 ± 0.19, and the mean ratio of sural nerve SNAP amplitude to DSN SNAP amplitude was 3.17 ± 1.33. These normative data of the DSN might be used as reference values for the study of this very distal peripheral nerve.

Nomogram for determining lower limit of the sural response

Age and height influence on sural sensory nerve action potential (SNAP) have been studied separately. Our aim was to develop an equation for predicting the lower normal limits as a function of both these factors. One hundred fifty-eight healthy volunteers, 63 male, with mean age 45.8 and mean height 167.3 without symptoms or signs of peripheral neuropathy participated in the study. The sural SNAP was recorded at the level of the ankle joint, just posterior to the lateral malleolus, using surface electrodes. Antidromic supramaximal stimulation was performed 13 cm proximally at the posterior midcalf. The mean sural SNAP amplitude was 19.9+/-6.89 microV. Pearson linear correlation showed a negative correlation of the SNAP amplitude with age (R=-0.22, p=0.005) and height (R=-0.19, p=0.03). The multiple linear regression model was applied for both parameters of age and height with SNAP amplitude as the dependent parameter, producing the following equation: SNAP amplitude=62.45-0.1447 x Age-0.2147 x Height. Using our normal data, the computed lower limits of the 95% prediction interval for the sural SNAP amplitude of an individual subject, depending on his age and height, were calculated. The individualized normal values provided by our equation are essential for the correct interpretation of sural nerve studies.

Prospective study of peripheral neuropathy in Machado–Joseph disease

Peripheral neuropathy (PN) has long been recognized in Machado-Joseph disease (MJD), but its natural history is an unsettled issue. Therefore, we prospectively assessed 40 with MJD for 13 months with nerve conduction (NC) studies and the revised total neuropathy score (TNSr) to study the progression of PN. There was no significant change in the TNSr score over the follow-up period. In contrast, the average sural sensory nerve action potential (SNAP) amplitude decreased significantly over the same interval from a mean of 13.2 muV to 9.8 muV (P < 0.001). There was an inverse correlation between the change in the sural SNAP amplitude and the length of the CAG triplet repeat expansion (r = 0.574, P < 0.001). The reduction in the mean sural SNAP amplitude also correlated with progression of ataxia. This indicates that PN progresses faster in individuals with larger (CAG)(n) expansions, and nerve conduction studies may be useful to study disease progression in MJD.

5. Sural and radial sensory responses in patients with sensory polyneuropathy

Introduction: The sural/radial nerve amplitude ratio (SRAR) is the quotient of the Sensory Nerve Action Potential (SNAP) amplitudes (Amp) of the sural and the superficial radial nerve. It has been hypothesized that this ratio can be used for the detection of early axonal loss; because the sural SNAP amplitude will decrease first, thereby also decreasing the SRAR value. Objectives: To determine the sensitivity and specificity of SRAR, age-adjusted sural and radial SNAP Amp in the diagnosis of axonal sensory polyneuropathy in cancer patients. Design: Retrospective review. Setting: Comprehensive cancer center.