Stage Of Polyneuropathy Research Articles

Neck triangle nerve enlargement in hereditary transthyretin amyloidosis correlates with changes in the autonomic, cardiac, and gastrointestinal systems.

Hereditary transthyretin amyloidosis (ATTRv) is a hereditary disease that affects multiple bodily systems. Although sonography generally reveals enlargement of nerves in the limbs, the brachial plexus, and vagus nerve, the clinical significance of these findings remains unclear. We performed sonographic measurements of the median nerve, cervical spinal nerves at the C5-C7 level, and the vagus nerve in patients with ATTRv and healthy controls. Clinical profiles and cardiac and gastrointestinal examination results were also collected for linear regression analysis. We recruited 47 patients with ATTRv (males/females: 34/13, age: 65.6±5.3 years). The sampled segments were all significantly larger than those of the controls. In the clinical profiles, the sum of the Z scores of the neck triangle nerves (cervical spinal nerves and vagus nerve) and of all nerves (cervical spinal nerves, vagus nerve, and median nerve at the wrist) significantly correlated with the familial amyloid polyneuropathy stage, onset of autonomic nervous system (ANS) symptoms, and autonomic symptom scores. On cardiac examinations, several ultrasonography and magnetic resonance imaging parameters (primarily those that reflect heart volume) were found to be significantly correlated with the sum of the Z scores of the cervical spinal nerves but not with the Z score of the vagus nerve. In gastrointestinal evaluation, the cross-sectional area of the vagus nerve was correlated with gastric emptying time parameters on scintigraphy. Neck triangle nerve enlargement on sonography correlated with parameters related to ANS dysfunction, indicating that nerve enlargement observed on ultrasonography may serve as a potential surrogate biomarker of ATTRv.

The use of a clinical calculator to determine the rate of development of chronic kidney disease in elderly patients with type 2 diabetes mellitus

Aim – to develop an applied prognostic calculator for the rate of progression of CKD in elderly patients with type 2 diabetes, which makes it possible to identify a group of high rate of GFR reduction in conditions of routine outpatient admission. Material and methods. 69 clinical indicators were studied, the interrelationships and significance of differences in parameters in the groups identified according to the original diagnostic parameter, the glomerular filtration rate reduction index with a threshold value of 3.83 ml/min/1.73 m2 per year, above which the rate of progression of CKD was considered high. Results. By using regression analysis, significant factors for the prognostic calculator were identified: the duration of diabetes and insulin therapy, concomitant diagnosis of obesity, pulse in the ankle artery, severe stage of polyneuropathy, risk group IV of hypertension, treatment with sulfonylureas, the number of antihypertensive drugs taken. When evaluating the information capacity and predictive ability of the calculator, the area under the AUC ROC curve was 0.89 (0.80; 0.99) p 0.001, which characterizes the quality of the diagnostic technique as high. Conclusion. The presented calculator gives the doctor the opportunity to identify a group of patients with the risk of rapid progression of CKD directly on an outpatient basis.

Altered gut microbiota in Taiwanese A97S predominant transthyretin amyloidosis with polyneuropathy

Increasing evidence suggests that gut microbiota alterations are related to development and phenotypes of many neuropsychiatric diseases. Here, we evaluated the fecal microbiota and its clinical correlates in patients with hereditary transthyretin amyloidosis (ATTRv) and polyneuropathy. Fecal microbiota from 38 ATTRv patients and 39 age-matched controls was analyzed by sequencing 16S V3–V4 ribosomal RNA, and its relationships with clinical characteristics of polyneuropathy and cardiomyopathy were explored. The familial amyloidotic polyneuropathy stage was stage I, II, and III in 13, 18, and 7 patients. 99mTc-PYP SPECT showed a visual score of 2 in 15 and 3 in 21 patients. The gut microbiota of ATTRv patients showed higher alpha diversity (ASV richness and Shannon effective numbers) and dissimilar beta diversity compared to controls. Relative abundance of microbiota was dominated by Firmicutes and decreased in Bacteroidetes in ATTRv patients than in controls. Patients with more myocardial amyloid deposition were associated with increased alpha diversity, and the abundance of Clostridia was significantly correlated with pathophysiology of polyneuropathy in ATTRv patients. These findings demonstrated alterations in the gut microbiota, especially Firmicutes, in ATTRv. The association between altered microbiota and phenotypes of cardiomyopathy and polyneuropathy might suggest potential contributions of gut microbiota to ATTRv pathogenesis.

IDF21-0671 Identification of neurophysiological abnormalities in nerve in patients with type 1 diabetes

Background: The progression of neuropathy is a continuum from subclinical neuropathy detectable with electrophysiological tests to clinically evident one recognizable on neurological examination. Although there has been considerable research of peripheral neuropathy in type 1 diabetes, still there is controversy regarding the pattern of nerve involvement in diabetic neuropathy. Detection of the pattern of nerve involvement can help to establish a protocol for screening of diabetic peripheral neuropathy (DPN) in its subclinical stage. Aim: The aim of this study was to describe the pattern of nerve involvement in type 1 diabetic patients with subclinical neuropathy using nerve conduction studies. Method: 65 patients with type 1 diabetes, ages from 18 to 55 years, and 34 controls without diabetes matched to the patient group were included into the study. All patients and controls underwent a standard neurological examination (NSS and NDS (the variant used in Belarus) score) and bilateral nerve conduction study (NCS) of the sensory and motor lower limb nerves using NeuroSoft machine. Interpretation of the results was based on the following normal reference ranges: n. Peroneus superficialis A> 10μV, v> 45 m/s; n Suralis A> 5 μV, v> 45 m / s; n Peroneus profundus A> 3mV, v> 40 m/s; n Tibialis A> 3.5mV, v> 40m/s. Data was analysed using IBM SPSS statistics v 20.0. Results: Clinically evident DPN was detected in 14 patients with type 1 diabetes from 65 examined. The use of NCS allowed to identify the subclinical stage of polyneuropathy (abnormalities in at least two of the electrophysiological parameters) additionally in 35 patients who had no symptoms and clinical signs of DPN. In all the patients of the control group, the NCS parameters were in the reference range. Regarding abnormal NCS parameters in patients with subclinical diabetic neuropathy (conduction velocity vs. amplitude of the compound action potential), amplitudes reduction for the n. Peroneus superficialis and n. Peroneus profundus predominated. Median of the amplitude for n. Peroneus superficialis in patients with subclinical diabetic polyneuropathy was 7.22 [5.25; 8.54] μV vs. 12.4 [10.57; 16.2] μV in the control group, p <0.001; for n. Peroneus profundus 2.21 [1.68; 2.68]mV vs. 3.15 [3.04; 3.42]mV in the control group, p <0.001. Significant differences in the amplitudes for n.Suralis and n.Tibialis has not been identified. Nerve conduction velocity (NCV) in both groups – in patients with the subclinical diabetic polyneuropathy and the control group – was within the reference range. However, the medians of NCV for n. Suralis and n. Tibialis were significantly lower in the group of patients with neuropathy compared with the controls – 47.08 [44.35; 50.13]m/s vs. 51.3 [47.6; 59.05]m/s, p = 0.025 and 44.8 [42.15; 48.2]m/s vs. 49.35 [48.30; 53.45]m/s, p = 0.004, respectively. Conclusion: In patients with type 1 diabetes with a subclinical stage of diabetic polyneuropathy the most frequent neurophysiological abnormalities were reduced amplitudes (the axonal damage) for sensory and motor fibers of n. Peroneus.

Optimal Screening Value of Vitamin D Deficiency for Distal Symmetric Polyneuropathy in Patients with Diabetes

Objective: The cut-off value of serum 25(OH)D level for bone-skeletal and cardiovascular diseases are well defined. However, there is no current study defining the optimal cut-off value of serum 25(OH)D levels for preventing diabetic distal symmetric polyneuropathy (DSP). We aimed to evaluate the relationship between the 25(OH)D levels and the parameters of electrophysiology and Toronto Clinical Scoring System (TCSS) to obtain a cut-off value of serum 25(OH)D levels in diabetic DSP patients. Methods: This is a case-control study included 90 diabetic patients with or without diagnosed DSP who were visiting the outpatient Physical Therapy and Rehabilitation Clinic. The patients’ demographic data and vitamin D levels were recorded. The patients were classified according to serum 25(OH)D levels as having optimal, insufficiency, and deficiency. The electrophysiological study was conducted for the diagnosis and staging of polyneuropathy. TCSS was used to evaluate the patients’ neuropathic symptoms. Results: From the results of this study conducted on the 90 patients that were diagnosed with diabetes, it was found that the electrophysiological study and TCSS were significantly different in the three vitamin D groups. Regression analysis test demonstrated that 25 (OH) D level with 0.845 odds ratio is the only risk factor for the development of DSP. The serum levels of 25(OH)D below 15/18 ng/mL is associated with DSP. Conclusion: This study indicate that vitamin D deficiency is a risk factor for the development of DSP, and serum 25(OH)D level ≤ 15 ng/ml is crucial in assessing the severity of neuropathic symptoms.

Role of interdigital sensory nerve conduction study as a noninvasive approach for early diagnosis of diabetic peripheral neuropathy.

Diabetes mellitus is amongst the most common causes of polyneuropathy worldwide that can eventually terminate to irreversible complications. The remarkable impact of diabetic polyneuropathy as a debilitating condition on the healthcare system and total costs of diabetes care is undeniable. Despite the existence of numerous diagnostic tools such as routine electrophysiologic procedures, its early detection is challenging. This study designed to compare more distal techniques of electrodiagnostic testing, including interdigital sensory nerve conduction studies (NCSs), with conventional approaches and to investigate its role in confirming the early stages of polyneuropathy. This cross-sectional study was performed in the Physical Medicine and Rehabilitation Department of Hazrat Fatemeh Reconstruction Surgery Hospital. Thirty one symptomatic diabetic outpatients and 23 asymptomatic nondiabetic subjects included in our study. We performed nerve conduction studies on five sensory nerves consist of the dorsal sural nerve, medial plantar nerve, digital branches of the interdigital nerves to toes I, II, and III (as a new antidromic technique). In this study, all techniques applied with a surface stimulator and pick-up electrodes. In the group of patients, 9 (29%) and 22 (71%) subjects had impaired and normal routine NCSs, respectively. Interestingly, the results of interdigital nerve studies were abnormal in the 17 out of 22 patients with normal routine NCSs. Also, 11 and 13 subjects had impaired medial plantar nerve and dorsal sural nerve conduction studies, respectively. Accordingly, with this new method, the prevalence of detectable diabetic neuropathy increased from 46% to 83%. We conducted this study intending to demonstrate the application of a new technique for early diagnosis of diabetic polyneuropathy, especially in the presymptomatic and subclinical neuropathies. The digital sensory branches of IDNs known as the most distal sensory nerves, which can be easily evaluated with new antidromic SNAP technique. Our method is simple, non-invasive, suitable, sensitive, and reproducible. There is no need to needle electrode or averaging technique to record an appropriate amplitude of IDN. Thus, it is recommended as a convenient electrophysiological option for early diagnosis of DPN.

Cardiac involvement, morbidity and mortality in hereditary transthyretin amyloidosis because of p.Glu89Gln mutation.

Hereditary transthyretin amyloidosis is a systemic infiltrative disease, caused by a mutation in the transthyretin gene. p.Glu89Gln is the most common mutation in the Balkan countries. We evaluated the clinical manifestations, cardiac involvement, morbidity and mortality in 78 patients with p.Glu89Gln mutation, verified through a DNA analysis. Clinical assessment, electrocardiogram and echocardiography were performed at the time of diagnosis. The patients have been followed for 30 months. All included patients were Caucasian, 39 (50%) - men, with median age at diagnosis of 56 years (42-73), median age at onset -- 53 years (35-69), starting significantly earlier in men (4.36, P = 0.004). Cardiac and neurological involvement was found in 74 (95%) patients. Pathological ECG was present in 65 (84%) patients, infarct pattern in 43 (56%), low voltage in 24 (31%). Echocardiography revealed an infiltrative cardiomyopathy with restrictive filling in 31 (40%) and ejection fraction less than 50% in 20 (27%) patients. Twenty-two patients (28%) died: 14 (64%) because of advanced heart failure, 6 (27%) died suddenly, 2 (9%) from an ischemic stroke. The median age at death was 58.5 years (52-72). No statistically significant sex difference in survival was observed; a significant difference in survival was found for the New York Heart Association class, familial amyloidotic polyneuropathy stage, ejection fraction, filling pattern and tafamidis treatment. Cardiac involvement is common and has significant prognostic implications in the evaluated patients with p.Glu89Gln mutation. Heart failure and rhythm disturbances are the main causes of death. An earlier identification of the disease is crucial to improve prognosis.

6MWT performance correlates with peripheral neuropathy but not with cardiac involvement in patients with hereditary transthyretin amyloidosis (hATTR)

Hereditary transthyretin amyloidosis (hATTR) is a life-threatening multisystemic disease with sensory-motor peripheral neuropathy, cardiomyopathy and dysautonomia. Although the six-minute walk test (6MWT) is one of the most popular clinical tests to assess functional exercise capacity in cardiopulmonary and neuromuscular diseases, little is known about 6MWT in evaluating hATTR patients. A prospective single-center pilot study was performed in twenty hATTR patients, comparing 6MWT with widely used outcome measures. After 18 months, fourteen patients were re-evaluated. 6MWT performance was highly related with familial amyloidotic polyneuropathy stage and polyneuropathy disability score, and with CMT examination score, neuropathy impairment score-lower limbs and Kumamoto score. There was no correlation with compound autonomic dysfunction test, modified body mass index and numerous indices of heart dysfunction. After 18 months, familial amyloidotic polyneuropathy stage and polyneuropathy disability score systems were not able to reveal any significant change, whereas all other outcome measures significantly worsened. Among the outcome measures monitoring the neuropathic disturbances, neuropathy impairment score-lower limbs showed the highest responsiveness to change (adjusted effect size: 0.79), followed by CMT examination score (0.67), Kumamoto scale (0.65), 6MWT (0.62). 10MWT showed a very small value (0.21). Compound autonomic dysfunction test had a large value (0.91) whereas modified body mass index a small/moderate value (0.49). 6MWT is a simple and sensitive tool to monitor neuropathic involvement but not cardiac dysfunction in hATTR course.

Effect of statins on oxidative DNA damage in diabetic polyneuropathy.

Oxidative stress induces nerve damage in type 2 diabetes mellitus and leads to diabetic polyneuropathy (DPN) and can affect the DNA and antioxidant status. Statins have pleiotropic, protective effects on the peripheral nerves of patients with diabetes. The aim of this study was to determine the effects of ezetimibe/simvastatin and rosuvastatin on DNA damage in patients with DPN. This randomized, double-blind, placebo-controlled, clinical trial comprised outpatients from Guadalajara, Mexico. The inclusion criteria were either gender, age 35–80 years, type 2 diabetes, glycated hemoglobin ≤10%, diabetic polyneuropathy stage 1/2, and signed informed consent. Patients who were taking antioxidant therapy or statins, had hypersensitivity to drugs, experienced organ failure, were pregnant or breastfeeding, or had other types of neuropathy were excluded. We assigned patients to placebo, ezetimibe/simvastatin 10/20 mg, or rosuvastatin 20 mg, and the primary outcomes were 8-hydroxy-2′-deoxyguanosine (8-OHdG) for DNA damage, 8-oxoguanine-DNA-N-glycosilase (hOGG1) for DNA repair, and superoxide dismutase (SOD). Seventy-four patients were recruited. Nine patients were included as negative controls. There were no differences in 8-OHdG between the healthy subjects (4.68 [3.53–6.38] ng/mL) and the DPN patients (4.51 [1.22–9.84] ng/mL), whereas the hOGG1 level was 0.39 (0.37–0.42) ng/mL in the healthy subjects and 0.41 (0.38–0.54) ng/mL in patients with DPN at baseline (p = 0.01). SOD decreased significantly in patients with DPN (5.35 [0.01–17.90] U/mL) compared with the healthy subjects (9.81 [8.66–12.61] U/mL) at baseline (p < 0.001). No significant changes in DNA biomarkers were observed in any group between baseline and final levels. We noted a rise in hOGG1 in patients with DPN, without modifications after treatment. There was a slight, albeit insignificant, increase in SOD in patients who were on statins.

Toronto Clinical Neuropathy Score is valid for a wide spectrum of polyneuropathies.

The Toronto Clinical Neuropathy Score (TCNS) is a valid and reliable scale for the diagnosis and staging of diabetic sensorimotor polyneuropathy. In this study, we aimed to explore the performance of the TCNS in non-diabetic polyneuropathies. We performed a prospective study from November 2016 to May 2017 of patients with non-diabetic polyneuropathy. Patients had clinical, electrophysiological and functional assessments of their polyneuropathy, and the findings were correlated with the TCNS. The TCNS correlated with all clinical, electrophysiological and disability measures of polyneuropathy, mostly at a moderate level (e.g. r = -0.58 for sural nerve action potential amplitude). Higher TCNS severity grades were associated with worse polyneuropathy on all measures in the lower limbs, and with worse electrophysiological parameters and vibration perception thresholds in the upper limbs. The scale also showed excellent reliability and accuracy (kappa, 0.92-0.93 for inter- and intra-observer reliability; area under the receiver operating characteristics curve, 0.93). The TCNS is a valid and reliable scale for a wide spectrum of polyneuropathies, and might be useful in clinical practise and research for the diagnosis and staging of polyneuropathy.

Lack of Definite Association of Vitamin D Deficiency with Diabetic Neuropathy. Investigation in Greek and in Bangladeshi Patients.

Determination of the 25(OH) vitamin D levels in Greek-born and in Bangladeshi immigrant patients in Greece with diabetes with and without polyneuropathy. The method for the detection and staging of polyneuropathy proposed by Dyck, 1988 was used. A total of 111 Bangladeshi immigrants and 101 Greek diabetic patients took part in the study. Vitamin D levels were significantly lower in Bangladeshi than in Greek diabetic patients, and were significantly lower in Greek patients with small-fiber neuropathy. In Bangladeshi patients, there was no statistically significant difference in the subgroup of patients with polyneuropathy in comparison to those without polyneuropathy. The association of vitamin D deficiency only with a small number of Greek patients with exclusively small-fiber neuropathy does not allow us to draw a definite conclusion on the role of vitamin D in the pathogenesis of diabetic neuropathy.

Diyabetes mellitusta iyi glisemik kontrol ile nöropati gelişimi önlenebilir mi?

Objective: In our study, we aimed to investigate the effect of insulin treatment on peripheral nerves in patients with diabetes mellitus (DM) who under the oral antidiabetic therapy changed to insulin treatment. Additionally, we have searched for answer to the question that could F response used for as a parameter on monitoring the course of polyneuropathy with glycemic control. F response which use in the detection of polyneuropathy has been emphasized in previous studies. Material and Method: Ten voluntary diabetic patients who received indication insulin treatment while being monitored with oral antidiabetic treatment and diagnosed according to the American Diabetes Association (ADA) criteria were included in our study. All our patients were outpatients of Sisli Etfal Training and Research Hospital Diabetes Mellitus Clinic. All patients were evaluated for neurological examination, serum glucose and HbA1c levels, total neuropathy score (TNS) and electrophysiological evaluations before insulin treatment and in the first and fourth week of the treatment. Results: Seven of patients were women and three of them were men. Age of patients were ranged from 40 to 69 and the mean age was 55±9.01. DM duration of patients ranged from 1 to 15 years (mean: 6.2±4.83). On the first Electrophysiologic evaluations of four patients were assessed within normal limits. We detected sensory polyneuropathy in lower extremities in five patients and a polyneuropathy syndrome which affecting sensory fibers in the upper extremity and both sensory and motor fibers in the lower extremities in the remaining patient. We observed particularly improvement the sensory conduction amplitude in the control electrophysiological evaluation of the patients with moderate neuropathy or without polyneuropathy but there was not a significant difference in control electrophysiological evaluation of the patients with severe polyneuropathy in the initial evaluation. Conclusion: After occurring severe polineuropathy syndrome there is not any improvement with good glicemic control whereas early stage of polyneuropathy.

Elevated Glycosylated Hemoglobin is Associated With Subclinical Neuropathy in Neurologically Asymptomatic Diabetic Patients: A Prospective Study

The association between poorly controlled diabetes and higher risk of polyneuropathy is well established. The American Diabetes Association recommends that glycosylated hemoglobin (HbA1c) should be less than 7%. Most previous studies, which reported HbA1c correlation with polyneuropathy, used higher HbA1c cut points and focused on neurologically symptomatic patients. This study evaluated the correlation of HbA1c levels, using the 7% cut point, with abnormal nerve conduction studies in diabetic patients in the subclinical stage of polyneuropathy. Fifty neurologically asymptomatic diabetic patients were included. HbA1c was measured at time of inclusion and 3 months later followed by nerve conduction studies. Univariate and multivariate analyses with logistic regression models were used to study the association of different patient characteristics with abnormal nerve conduction studies. Fifteen women and 35 men were studied. Half of patients had elevated HbA1c and half had HbA1c <7%. Twenty-six patients (52%) had subclinical neuropathy (18 men, 8 women). In multivariate analysis, HbA1c was the most important factor predicting higher risk of subclinical neuropathy [adjusted odds ratio 10.71 (2.49, 46.01), P < 0.005]. Therefore, nerve conduction studies abnormalities commonly exist in diabetic patients in the subclinical stages of polyneuropathy, and are highly correlated to HbA1c levels. Therapies for diabetic neuropathy should target the early stages of the disease.

P123 MUAP configuration in different stages of polyneuropathy: Improved evaluation by registration from the cannula of a concentric EMG electrode?

The purpose of this study was to investigate whether age-related changes in motor unit (MU) contractile properties are reflected in parameters of motor unit action potentials (MUAPs). MUs of the medial gastrocnemius muscle were functionally isolated in anaesthetized Wistar rats. A control group of young animals (5–10 mo) was compared to two groups of old rats (24–25 mo and 28–30 mo). The basic contractile properties of MUs as well as the amplitude, total duration, peak-to-peak time, and number of turns within MUAPs were measured. Effects of aging were mainly observed for fast fatigable MUs (a prolongation of MUAPs and increased number of turns). The MUAP amplitude did not change significantly with aging in either MU type, but it correlated to the twitch or tetanic forces, which tended to increase with age, especially for slow MUs. We concluded that the prolongation of MUAPs and the greater incidence of signal turns was probably a result of a decrease in muscle fiber conduction velocity and/or an increase in their dispersion, and enlargement of MU territories – presumably caused by axonal sprouting of surviving motoneurons. The latter might also be responsible for the observed age-related tendency for a increase in MUAP amplitudes in slow MUs.

Stimulation of sudomotor axon reflex mechanism by carbachol in healthy subjects and patients suffering from diabetic polyneuropathy.

Sudomotor axon reflex (SAR) mechanism was stimulated by percutaneous iontophoresis of carbachol in healthy subjects and patients suffering from diabetic polyneuropathy (PNP) of differing severity (stage I-III). SAR response was assessed by hygrometry and compared with histamine induced neurogenic vasodilation (laser-Doppler flowmetry) and itching sensation (visual analogue scale), which may provide information on neuro-secretion and afferent function of nociceptive unmyelinated nerve fibers. Carbachol induced long lasting SAR response with maximal sweating rates 20-30 minutes after stimulus onset. In diabetic patients the carbachol induced SAR response and the histamine induced itching sensation were significantly reduced in stage III of PNP. In contrast, histamine induced vasodilatation was significantly impaired in all stages of PNP. It is concluded that prolonged SAR response following iontophoresis of carbachol can simplify evaluation of sudomotor function when compared to established tests using intradermal application of acetylcholine. Furthermore, to demonstrate impairment of unmyelinated nerve fibers in PNP, histamine induced vasodilatation was found to be more sensitive than SAR response.

The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study.

The magnitude of the health problem from diabetic neuropathies remains inadequately estimated due to the lack of prospective population-based studies employing standardized and validated assessments of the type and stage of neuropathy as compared with background frequency. All Rochester, Minnesota, residents with diabetes mellitus on January 1, 1986, were invited to participate in a cross-sectional and longitudinal study of diabetic neuropathies (and also of other microvascular and macrovascular complications). Of 64,573 inhabitants on January 1, 1986 in Rochester, 870 (1.3%) had clinically recognized diabetes mellitus (National Diabetes Data Group criteria), of whom 380 were enrolled in the Rochester Diabetic Neuropathy Study. Of these, 102 (26.8%) had insulin-dependent diabetes mellitus (IDDM), and 278 (73.2%) had non-insulin-dependent diabetes mellitus (NIDDM). Approximately 10% of diabetic patients had neurologic deficits attributable to nondiabetic causes. Sixty-six percent of IDDM patients had some form of neuropathy; the frequencies of individual types were as follows: polyneuropathy, 54%; carpal tunnel syndrome, asymptomatic, 22%, and symptomatic, 11%; visceral autonomic neuropathy, 7%, and other varieties, 3%. Among NIDDM patients, 59% had various neuropathies; the individual percentages were 45%, 29%, 6%, 5%, and 3%. Symptomatic degrees of polyneuropathy occurred in only 15% of IDDM and 13% of NIDDM patients. The more severe stage of polyneuropathy, to the point that patients were unable to walk on their heels and also had distal sensory and autonomic deficits (stage 2b) occurred even less frequently--6% of IDDM and 1% of NIDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Detection, characterization, and staging of polyneuropathy: assessed in diabetics.

The reported prevalence of diabetic polyneuropathy varies from 5 to 80%. This unsatisfactory state may relate to evaluation of different patient groups, different minimal criteria for the diagnosis of neuropathy, and different degrees of surveillance. To made matters worse, patients with polyneuropathy tend to be equated ignoring differences in severity. To remedy this situation, four recommendations are made: (1) population-based patients should be studied, (2) nerve conduction should be used to set minimal criteria for neuropathy because the test is objective, sensitive, and repeatable, (3) validated tests of symptoms and deficits should also be used because clinical manifestations of neuropathy cannot be accurately inferred from electrophysiologic measurements, and (4) approaches to staging severity of neuropathy should be developed and used in expressing abnormality. To this end minimal criteria for the diagnosis of diabetic polyneuropathy have been proposed, and validated tests to assess neuropathic symptoms and sensory deficits have been developed. In this report we also propose a staging approach utilizing nerve conduction and neurologic history and examination and validated tests of neuropathic symptoms and deficits.