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PubMed2003

Sympathetic mediated vasomotion and skin capillary permeability in diabetic patients with peripheral neuropathy.

AIMS/HYPOTHESIS: A loss of sympathetic function could lead to changes in capillary fluid filtration in diabetic patients. We investigated whether a decreased sympathetically mediated vasomotion in the skin in diabetic patients with peripheral neuropathy is associated with an abnormal capillary leakage. METHODS: Three matched groups were studied: 18 diabetic patients with documented peripheral neuropathy (DN), 18 diabetic patients without peripheral neuropathy (D), and 18 healthy control subjects (C). Sensory and motor nerve function of the distal extremities were assessed by standard neurography, and expressed in a sensory-motor nerve function score. Sympathetic vasomotion of the skin microcirculation was assessed by determining the power of blood flow variability in the low-frequency (0.02-0.14 Hz) band by spectral analysis of laser Doppler flowmetry at the median ankle. Skin capillary leakage was evaluated by sodium fluorescein videodensitometry at the same site of the foot. RESULTS: Sympathetically mediated vasomotion of the foot skin microcirculation was lower in diabetic patients with documented peripheral neuropathy compared with diabetic patients without peripheral neuropathy and control subjects (p<0.001). Capillary sodium fluorescein leakage was larger in 18 diabetic patients with documented peripheral neuropathy than in diabetic patients without peripheral neuropathy (p<0.02) and C (p<0.005). Multiple regression analysis disclosed that a reduced sympathetically mediated vasomotion, together with a lower sensory-motor nerve function score, independently contributed to the variance in sodium fluorescein leakage, for 30% (p<0.001) and 17% (p<0.01), respectively. CONCLUSIONS: A loss of sympathetic tone, apart from sensory-motor nerve dysfunction, seems to be a major determinant of an increased capillary permeability in diabetic patients with neuropathy.

Capillary Permeability↗
PubMed1999

Quantitative sensory testing and risk factors of diabetic sensory neuropathy.

The goal of this study was to identify risk factors for diabetic peripheral sensory neuropathy in type 2 diabetes mellitus in a Chinese population. Peripheral sensory neuropathy was detected by quantitative sensory testing (5.07/10 g monofilament, neurometer and 128-Hz Riedel Seiffert graduated tuning fork). Those who had two or more abnormal quantitative sensory testings were defined as having diabetic sensory neuropathy. Of the 558 non-insulin dependent diabetes mellitits subjects, 62 (11.1%) had peripheral neuropathy. In 59 (10.6%) detection was by monofilament testing, 45 (8.1%) by graduated tuning fork, and 189 (33.9%) by neurometer. In a multivariate logistic regression model, age and insulin therapy were significantly associated with peripheral neuropathy. Age, serum triglyceride, height, and fasting plasma glucose were independently associated with large fiber neuropathy. Our results confirm the previously identified multiple risk factors of diabetic neuropathy. Different quantitative sensory testings detect different nerve fiber defects. The weak correlation between these tests indicates the need to use more than one test in screening for diabetic neuropathy.

Aged↗
PubMed1993

Somatic pain threshold and reactive hyperemia in autonomic diabetic neuropathy and silent myocardial ischemia.

In 31 patients with coronary artery disease (autonomic neuropathy, n = 11; diabetes without neuropathy, n = 10; silent myocardial ischemia without diabetes, n = 10) difference in somatic pain threshold and plethysmographically determined reactive hyperemia induced by forearm skeletal muscle ischemia was investigated. There was no difference in reactive hyperemia after passive maximum forearm ischemia in the three groups indicating identical vascular reactivity. After symptom-limited ischemic work however, reactive hyperemia was significantly higher in patients with silent myocardial ischemia as compared to diabetic patients. Exercise time was longer in patients with silent myocardial ischemia (153 +/- 51 s) as in patients with diabetic neuropathy (139 +/- 45 s) and diabetics without neuropathy (120 +/- 45 s). Pain as a cause of termination of symptom-limited ischemic forearm exercise occurred less frequently in patients with diabetic neuropathy (2/11) and patients with silent myocardial ischemia (3/10) as compared to patients with diabetes without neuropathy (9/10). In conclusion, patients with silent myocardial ischemia have a higher ischemic tolerance in the working forearm as compared to diabetic patients with and without neuropathy. There is a quantitative difference in ischemic tolerance between patients with silent myocardial ischemia and patients with diabetic neuropathy.

Autonomic Nervous System Diseases↗
PubMed1995

Memory dysfunction and autonomic neuropathy in non-insulin-dependent (type 2) diabetic patients.

Considering the nervous system as a unit, it might be expected that diabetic patients with autonomic neuropathy could have a central abnormality expressed as cognitive dysfunction. To determine whether autonomic neuropathy is independently associated with cognitive dysfunction, we studied a cross-section of 20 non-insulin-dependent diabetic patients with autonomic neuropathy (14 males and six females; age (mean) = 60 + or - 1 years); 29 non-insulin-dependent diabetic patients without autonomic neuropathy (14 males and 15 females; age = 59 + or - 1 years) and 34 non-diabetic patients (10 males and 24 females; age = 58 + or - 1 years), matched by age, education and duration of disease. Cognitive function was evaluated by tests of immediate, recent and remote memory: verbal (digit span; word span) and visual (recognition of towers and famous faces). Diabetic patients with autonomic neuropathy scored (median) lower in visual memory tests than diabetic patients without autonomic neuropathy and controls (towers immediate = 5 versus 7 and 6; towers recent = 4 versus 6 and 6; faces = 16 versus 18 and 18; respectively; Kruskal-Wallis; P < 0.05). There was no difference in verbal memory performance (Kruskal-Wallis; P > 0.05). Entering age, education, duration of disease and fasting plasma glucose in a stepwise multiple regression, the performance in these tests remained associated with autonomic neuropathy (towers immediate, P = 0.0054, partial r2 = 0.166; towers recent, P = 0.0076, partial r2 = 0.163). Scores in visual tests correlated negatively with the number of abnormal cardiovascular tests (faces, r = -0.25; towers recent, r = -0.24; Spearman; P < 0.05). Decreased visual cognitive function in non-insulin-dependent diabetic patients is associated with the presence and degree of autonomic neuropathy.

Adult↗
PubMed1993

Noninvasive assessment of cardiac diabetic neuropathy by carbon-11 hydroxyephedrine and positron emission tomography.

OBJECTIVES: The purpose of this investigation was to evaluate the sympathetic nervous system of the heart by positron emission tomographic (PET) imaging in patients with diabetes mellitus with and without diabetic autonomic neuropathy. BACKGROUND: The clinical assessment of cardiac involvement in diabetic autonomic neuropathy has been limited to cardiovascular reflex testing. With the recent introduction of radiolabeled catecholamines such as carbon (C)-11 hydroxyephedrine, the sympathetic innervation of the heart can be specifically visualized with PET imaging. METHODS: Positron emission tomographic imaging was performed with C-11 hydroxyephedrine and rest myocardial blood flow imaging with nitrogen-13 ammonia. Three patient groups were studied, including healthy volunteers as control subjects, diabetic patients with normal autonomic function testing and diabetic patients with varying severity of autonomic neuropathy. Homogeneity of cardiac tracer retention as well as absolute tracer retention was determined by relating myocardial tracer retention to an arterial C-11 activity input function. RESULTS: Abnormal regional C-11 hydroxyephedrine retention was seen in seven of eight patients with autonomic neuropathy. Relative tracer retention was significantly reduced in apical, inferior and lateral segments. The extent of the abnormality correlated with the severity of conventional markers of autonomic dysfunction. Absolute myocardial tracer retention index measurements showed a 45 +/- 21% decrease in distal compared with proximal myocardial segments in autonomic neuropathy (0.069 +/- 0.037 min-1 vs. 0.13 +/- 0.052 min-1, p = 0.02). CONCLUSIONS: This study demonstrates a heterogeneous pattern of neuronal abnormalities in patients with diabetic cardiac neuropathy. The extent of this abnormality correlated with the severity of neuropathy assessed by conventional tests. Future studies in larger groups of patients are required to define the relative sensitivity of this imaging approach in detecting cardiac neuropathy and to determine the clinical significance of these scintigraphic findings in comparison with conventional markers of autonomic innervation.

Adult↗
PubMed1998

Does peripheral neuropathy invariably accompany nephropathy in type 1 diabetes mellitus?

In patients with Type 1 diabetes mellitus complicated by diabetic nephropathy and retinopathy, it is usually believed that significant neuropathy is almost universal, but few studies have directly addressed this. This study assessed neuropathy in 91 such subjects, using vibration perception thresholds (VPT) and the neuropathy disability score (NDS). A total of 34% of subjects had no neuropathy on age adjusted VPT (z score) and 26% had no neuropathy on NDS. The severity of neuropathy as measured by VPT z score was related to increasing glycated haemoglobin (P = 0.02) and male sex (P = 0.03), and NDS was independently associated with age (P < 0.0001) and HbA1c (P = 0.003). These factors together accounted for only 12 and 31% of the total variance in VPT z score and NDS, respectively. In conclusion, the study has shown that a significant proportion of patients with diabetic nephropathy are free of neuropathy, but the full explanation for their protection from neuropathy is unclear.

Adult↗
PubMed1999

Prevalence of peripheral neuropathy with insulin-dependent diabetes mellitus.

Insulin-dependent diabetes mellitus (IDDM) is rare in Chinese children. There have been no reports on the prevalence of peripheral neuropathy in Chinese children with IDDM. This study aimed to determine prevalence of subclinical peripheral neuropathy in Chinese children with IDDM. Motor and sensory nerve conduction studies of both median, ulnar, peroneal, and tibial (motor nerves) and median, ulnar, and sural (sensory nerves) were performed in 38 children with IDDM (18 males, 20 females). The age was 4-21 years (mean = 12.7 years; median = 12 years, 6 months). The duration of diabetes was less than 5 years in 15, 5-10 years in 14, and more than 10 years in nine. Neurophysiologic evidence of subclinical peripheral neuropathy was present in 26 patients (68.4%) of which motor, sensory, or motor and sensory involvement was 26 (68.4%), eight (21.1%), and 26 (68.4%), respectively. Twelve (31.6%) and 14 (36.8%) children had mild and moderate degrees of peripheral neuropathy, respectively. Among the 26 children with abnormal nerve-conduction studies, two (7.7%) had symptoms of numbness and pain in the lower limbs. Thus, two children had symptomatic neuropathy and most (n = 24) had asymptomatic peripheral neuropathy. Two children had systemic hypertension, and one (3.8%) had laboratory evidence of early renal complications. Analysis of demographic and laboratory risk factors for the development of subclinical peripheral neuropathy revealed that the age of onset, duration of diabetes, level of hemoglobin A1c, triglyceride, cholesterol, serum creatinine, and urea, microalbumin/creatinine ratio, and urinary microalbumin excretion rate were significantly related to the development of subclinical peripheral neuropathy in specific nerves.

Adolescent↗
PubMedDate not supplied

Relationship of medial arterial calcinosis to autonomic neuropathy and adverse outcomes in a diabetic veteran population.

STATEMENT OF THE PROBLEM: Medial arterial calcinosis (MAC) is associated with neuropathy, amputation, and mortality through an unknown mechanism. We hypothesized that MAC was a marker of autonomic neuropathy rather than a risk factor and that the outcomes were due to autonomic neuropathy. METHODS: All subjects in an ongoing prospective study of diabetic foot conditions in a diabetic veteran cohort who received a foot radiograph between 11/7/90 and 11/5/93 were included. Autonomic neuropathy measured as either heart rate variability with timed respiration or postural hypotension. A logistic model predicted the presence of MAC at baseline and Cox proportional models assessed the relative contribution of autonomic neuropathy and traditional risk factors for the outcomes of ulceration, amputation, and death. RESULTS: MAC was identified in 181 subjects, no MAC in 253 subjects, and 39 were excluded due to disagreement between observers. Both measures of autonomic neuropathy were independent predictors of MAC at baseline, even after adjustment for vibration sensation loss in a logistic model. MAC was associated with an increased risk for ulceration (hazards ratio, HR: 2.1, 95% confidence intervals, CI, 1.4-3.1), amputation (HR 3.3, 95% CI 1.5-7.4), and mortality (HR 1.6, 95% CI 1.1-2.2). The addition of either autonomic measure of neuropathy did not change the MAC HR or significantly improved the fit of the model. CONCLUSIONS: Our hypothesis that the excess mortality, amputation, and ulceration in persons with MAC could be explained by autonomic neuropathy measured as postural hypotension or heart rate variability with measured respiration was not supported.

Age of Onset↗
PubMed2003

Management of neuropathy and foot problems in diabetic patients.

Diabetic neuropathy (DN) is a complex set of clinical syndromes that affect distinct regions of the nervous system, either singly or combined. DN is the most common form of neuropathy in the developed countries of the world and is responsible for 50% to 75% of nontraumatic amputations. It is also the most life damaging--once autonomic neuropathy sets in, the mortality rate approximates 25% to 50% within 5 to 10 years. Distal symmetric polyneuropathy, the most common form of DN, usually involves both small and large nerve fiber damage. Small nerve fiber neuropathies occur early and are often present without objective signs or electrophysiologic evidence of nerve damage. The greatest risk is foot ulceration and subsequent gangrene. Large nerve fiber neuropathies, which involve the sensory and motor nerves, are generally neuropathies of signs rather than symptoms. Clinical presentation usually includes a "glove and stocking" distribution of sensory loss and the greatest risk is Charcot's neuroarthropathy. Diagnosis of DN relies heavily on a careful patient history and physical examination. Most critical is that both the patient and the patient's shoes should be examined and corrective measures taken. Several studies have shown that good diabetes control can significantly reduce neuropathy. As new drugs and ways to enhance nerve blood flow and block pain pathways at different levels are being explored, the effective treatment of DN and the reduction of its impact on quality of life as well as mortality will become a reality. Patient education and preventive strategies, however, are still the best ways to treat the complications of neuropathy and reduce the amputation rate.

Amputation, Surgical↗
PubMed1997

Corrected QT interval in relation to the severity of diabetic autonomic neuropathy.

The aim of this study was to investigate to what extent the existence of objective signs of diabetic autonomic neuropathy affects the corrected QT interval (QTc) in diabetic subjects. A total of 105 diabetic subjects (type 1, n = 53; type 2, n = 52) as well as 40 matched (by age and sex) control subjects were studied. All subjects underwent the battery of five Ewing tests. Autonomic neuropathy was diagnosed if two of the five tests were abnormal. In addition, the result of each test was considered as normal (grade = 0), borderline (grade = 1) or abnormal (grade = 2), and on the basis of the sum of the scores we calculated a total score for autonomic neuropathy. The QTc interval was measured at rest, and a value > 440 ms was considered abnormal. The QTc interval was significantly more prolonged in diabetic persons with autonomic neuropathy than in those without neutopathy and in control subjects: 408.4 +/- 24.2 ms vs. 394.6 +/- 27.9 ms and 393.6 +/- 25.5 ms respectively (P = 0.001). Furthermore, multivariate analysis controlling for age, sex, systolic and diastolic blood pressure, body mass index (BMI), waist-hip ratio (WHR), smoking, type and duration of diabetes, type of treatment, HBA1c and total score of autonomic neuropathy eliminated the role of all these factors as potential confounders except for the total score of autonomic neuropathy, which was found to affect QTc interval independently and significantly (P = 0.012). In summary, the present study confirmed the well-known relation between autonomic neuropathy and QTc interval; in addition, it showed that QTc prolongation is associated with major degrees of autonomic neuropathy.

Adult↗
PubMed2001

Relation between homocysteinaemia and diabetic neuropathy in patients with Type 2 diabetes mellitus.

AIMS: Limited data are available on determinants of diabetic neuropathy as its pathogenesis is multifactorial. Since homocysteine exhibits toxic effects on vascular endothelial cells, the association between homocysteine and the prevalence of neuropathy in Type 2 diabetes mellitus was investigated. METHODS: A total of 65 Type 2 diabetic patients were consecutively enrolled into the study. Neuropathy was diagnosed according to clinical symptoms, clinical examination, electrophysiological sensory testing and autonomic function testing. With regard to homocysteine-related parameters, plasma homocysteine, folate, vitamin B12, vitamin B6 and renal function (creatinine, ceratinine clearance, cystatin C) were measured, and the C677T polymorphism of the methylenetetrahydrofolate reductase gene was determined. RESULTS: Forty-three of the Type 2 diabetic patients were classified as suffering from neuropathy. Both patient groups were comparable with regard to demographic data, blood pressure, glucose metabolism, renal function and homocysteine-related vitamins. In contrast, homocysteine levels (P = 0.04) and the frequency of hyperhomocysteinemia (>or= 15 micromol/l) (P = 0.01) were significantly increased in neuropathic patients. In a logistic regression model with neuropathy as dependent variable, homocysteine (adjusted for creatinine, homocysteine-related vitamins, HbA1c and duration of diabetes) was the only significant variable associated with the prevalence of neuropathy (odds ratio for homocysteine per 5 micromol/l increase: 2.60 (95% confidence interval 1.07-6.33)). CONCLUSION: The data indicate that homocysteine is independently associated with the prevalence of diabetic neuropathy in a collective of Type 2 diabetic patients. A larger, prospective study would be desirable to clarify the role of homocysteine in the pathogenesis of diabetic neuropathy.

Adult↗
PubMed1999

Inherited peripheral neuropathy.

Hereditary disorders of the peripheral nerves constitute a group of frequently encountered neurological diseases. Charcot-Marie-Tooth neuropathy type 1 (CMT1) is genetically heterogeneous and characterized by demyelination with moderately to severely reduced nerve conduction velocities, absent muscle stretch reflexes and onion bulb formation. Genetic loci for CMT1 map to chromosome 17 (CMT1A), chromosome 1 (CMT1B), and another unknown autosome (CMT1C). CMT1A is most often associated with a tandem 1.5-megabase (Mb) duplication in chromosome 17p11.2-12, or in rare patients may result from a point mutation in the peripheral myelin protein-22 (PMP22) gene. CMT1 B result from point mutations in the myelin protein zero (Po or MPZ) gene. The molecular defect in CMT1 C is unknown. Mutations in the early growth response 2 gene (EGR2) are also associated with demyelinating neuropathy. Other rare forms of demyelinating peripheral neuropathies map to chromosome 8q, 10q, and 11q. X-linked Charcot-Marie-Tooth neuropathy (CMTX), which has clinical features similar to CMT1, is associated with mutations in the connexin32 gene. Charcot-Marie-Tooth neuropathy type 2 (CMT2) is characterized by normal or mildly reduced nerve conduction velocity with decreased amplitude and axonal loss without hypertrophic features. One form of CMT2 maps to chromosome 1 p36 (CMT2A), another to chromosome 3p (CMT2B) and another to 7p (CMT2D). Dejerine-Sottas disease (DSD), also called hereditary motor and sensory neuropathy type III (HMSNIII), is a severe, infantile-onset demyelinating polyneuropathy that may be associated with point mutations in either the PMP22 gene or the Po gene and shares considerable clinical and pathological features with CMT1. Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder that results in a recurrent, episodic demyelinating neuropathy. HNPP is associated with a 1.5-Mb deletion in chromosome 17p11.2-12 and results from reduced expression of the PMP22 gene. CMT1A and HNPP are reciprocal duplication/deletion syndromes originating from unequal crossover during germ cell meiosis.

Charcot-Marie-Tooth Disease↗
PubMed2000

Autoantibodies to ganglionic acetylcholine receptors in autoimmune autonomic neuropathies.

BACKGROUND: Idiopathic autonomic neuropathy is a severe, subacute disorder with a presumed autoimmune basis. It is indistinguishable from the subacute autonomic neuropathy that may accompany lung cancer or other tumors. Autoantibodies specific for nicotinic acetylcholine receptors in the autonomic ganglia are potentially pathogenic and may serve as serologic markers of various forms of autoimmune autonomic neuropathy. METHODS: We tested serum from 157 patients with a variety of types of dysautonomia. Immunoprecipitation assays with iodine-125-labeled epibatidine and solubilized human neuroblastoma acetylcholine receptors were used to detect autoantibodies that bound to or blocked ganglionic receptors. RESULTS: Ganglionic-receptor-binding antibodies were found in 19 of 46 patients with idiopathic or paraneoplastic autonomic neuropathy (41 percent), in 6 of 67 patients with postural tachycardia syndrome, idiopathic gastrointestinal dysmotility, or diabetic autonomic neuropathy (9 percent), and in none of 44 patients with other autonomic disorders. High levels of the binding antibodies correlated with more severe autonomic dysfunction (including the presence of tonic pupils). Levels of these antibodies decreased in patients who had clinical improvement. All seven patients with ganglionic-receptor-blocking antibodies had ganglionic-receptor-binding antibodies and had idiopathic or paraneoplastic autonomic neuropathy. CONCLUSIONS: Seropositivity for antibodies that bind to or block ganglionic acetylcholine receptors identifies patients with various forms of autoimmune autonomic neuropathy and distinguishes these disorders from other types of dysautonomia. The positive correlation between high levels of ganglionic-receptor antibodies and the severity of autonomic dysfunction suggests that the antibodies have a pathogenic role in these types of neuropathy.

Adult↗
PubMed2004

Cardiac autonomic balance and QT dispersion during head-up tilt testing in diabetics with and without sensory neuropathy.

BACKGROUND: Cardiovascular autonomic dysfunction is associated with higher mortality in diabetics. However, detection methods of early cardiac diabetic dysautonomia, and its correlation with severity of sensory neuropathy, have not been described. METHODS: We analyzed the heart rate variability (HRV) by spectral analysis and QT dispersion in 23 diabetics with and without sensory neuropathy, and in 5 age-matched controls, in the supine position and during head-up tilt testing (HUT). Diabetics were divided into 3 groups according to the degree of sensory neuropathy. RESULTS: In the spectral analysis of HRV, the high frequency components in the supine position decreased as a function of severity of the neuropathy. High frequency in diabetics was significantly decreased in the supine position, even in absence of sensory neuropathy. The low/high frequency ratio (L/H) in the supine position was similar among controls and the 3 patient groups. L/H in diabetics with moderate or severe neuropathy did not increase from the supine to the upright position. Baseline QT dispersion increased proportionally to the severity of sensory neuropathy and, in patients without apparent sensory neuropathy, QT dispersion increased significantly during HUT. CONCLUSIONS: The spectral analysis of HRV and measurements of QT dispersion, before and during HUT, were reliable detection methods of early abnormalities in autonomic balance and may predict a risk of sudden cardiac death in diabetics.

Aged↗
PubMed2005

Reversal of diabetic peripheral neuropathy with phototherapy (MIRE) decreases falls and the fear of falling and improves activities of daily living in seniors.

OBJECTIVE: to determine whether restoration of sensation, impaired due to diabetic peripheral neuropathy (DPN), would reduce the number of falls and the fear of falling and improve activities of daily living (ADL) in a Medicare-aged population. DESIGN: retrospective cohort study of patients with documented, monochromatic near-infrared phototherapy (MIRE)-mediated, symptomatic reversal of DPN. SETTING: responses to a health status questionnaire following symptomatic reversal of DPN. PATIENTS: 252 patients (mean age 76 years) provided health information following symptomatic reversal of diabetic neuropathy (mean duration 8.6 months). MAIN RESULTS: incidence of falls and fear of falling decreased within 1 month after reversal of peripheral neuropathy and remained low after 1 year. Likewise, improved ADL were evident soon after reversal of peripheral neuropathy and showed further improvement after 1 year. Overall, reversal of peripheral neuropathy in a clinician's office and subsequent use of MIRE at home was associated with a 78% reduction in falls, a 79% decrease in balance-related fear of falling and a 72% increase in ADL (P < 0.0002 for all results). CONCLUSIONS: reversal of peripheral neuropathy is associated with an immediate reduction in the absolute number of falls, a reduced fear of falling and improved ADL. These results suggest that symptomatic reversal of diabetic neuropathy will have a substantial favourable, long-term socioeconomic impact on patients with DPN and the Medicare system, and improve the quality of life for elderly patients with diabetes and peripheral neuropathy.

Accidental Falls↗
PubMed2006

Peripheral insensate neuropathy--a tall problem for US adults?

The relation between height and lower extremity peripheral insensate neuropathy among persons with and without diabetes was examined by use of the 1999-2002 US National Health and Nutrition Examination Survey with 5,229 subjects aged 40 or more years. A monofilament was used to determine whether any of three areas on each foot were insensate. Peripheral insensate neuropathy was defined as the presence of one or more insensate areas. Its prevalence was nearly twice as high among persons with diabetes (21.2%) as among those without diabetes (11.5%; p < 0.001). Men (16.2%) had 1.7 times the prevalence of peripheral insensate neuropathy as did women (9.4%), but the difference was not significant after adjustment for height. Greater height was associated with increased peripheral insensate neuropathy prevalence among persons with and without diabetes (p < 0.001). This association was characterized by a sharp increase in prevalence among persons who were taller than 175.5 cm. Peripheral insensate neuropathy risk was significantly higher among those taller than 175.5 cm (adjusted odds ratio = 2.3, 95% confidence interval: 1.5, 3.5). The authors conclude that body height is an important correlate of peripheral insensate neuropathy. This association largely accounts for the difference in peripheral insensate neuropathy prevalence between men and women. Height may help health-care providers to identify persons at high risk of peripheral insensate neuropathy.

Body Height↗
PubMed1990

Sensory neuropathy in non-insulin-dependent diabetes mellitus. The San Luis Valley Diabetes Study.

A screening neurologic examination capable of detecting distal symmetric (sensory) neuropathy in a large population-based study of non-insulin-dependent diabetes mellitus in San Luis Valley, Colorado, in 1984-1986 is described and validated. The examination, completed in 279 diabetics and 577 controls, had 90% agreement with a standard neurologic examination completed on a subsample of 38 patients. Independent validation of neuropathy status was obtained with the Optacon tactile (vibration) stimulator. Mean, age-adjusted vibration threshold was significantly greater in those with neuropathy than in those without. The subtests of the examination most sensitive in detecting neuropathy were a combination of a positive history of neuropathy symptoms and decreased or absent deep tendon reflexes in both ankles. Age-adjusted prevalence of neuropathy in controls, those with impaired glucose tolerance, and diabetics was 3.9%, 11.2%, and 25.8%, respectively. Prevalence odds ratios were 3.5 and 10.6 for the presence of neuropathy in persons with impaired glucose tolerance and diabetes, respectively, compared with persons with normal glucose tolerance. Neuropathy was significantly associated with age, duration of diabetes, male sex, and glycemic control, but not with Anglo/Hispanic status.

Adult↗
PubMed2003

Painful neuropathies.

PURPOSE OF REVIEW: To summarize the current understanding of clinical assessment, pathophysiology, and treatment of pain in neuropathies, focusing on selected entities in which the understanding of the mechanisms underlying pain has advanced recently. RECENT FINDINGS: Ongoing studies are classifying the symptoms and signs of painful neuropathies, assuming that this approach may indicate particular pathomechanisms leading to more rational treatment. Nerve injury induces a large number of cellular changes, the relevance of which for the occurrence of pain is still under investigation. In models of diabetic neuropathy, an altered distribution of sodium channels, hyperexcitability of neurons, and changes in spinal connectivity seem to underlie the development of pain. The role of inflammatory mediators has been explored in inflammatory and degenerative neuropathies. Second messenger pathways contributing to hyperalgesia in various neuropathies have been identified, opening up new treatment options. A number of newer and older drugs have been studied for their use in painful neuropathies in clinical trials. Epidemiology has shown that, despite the availability of drugs with moderate efficacy in the treatment of neuropathic pain, a large percentage of patients do not gain access to them. SUMMARY: Advances in the standardization of assessment of patients with painful neuropathies are beginning to have an impact on how clinical studies are designed. Major progress has been made in the understanding of cellular and molecular changes after nerve injury, but their relevance for the pathophysiology of pain in neuropathies has still to be determined.

Antineoplastic Agents↗