Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuropathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMed2005

The effect of pancreatic islet transplantation on progression of diabetic retinopathy and neuropathy.

INTRODUCTION: Pancreatic islet transplantation (PIT) has only become an effective treatment for type 1 diabetes mellitus within the past 4 years. As a result, the long-term effects of PIT on progression of diabetic neuropathy and retinopathy are unknown. The benefit of halting or improving diabetic neuropathy and retinopathy is of particular interest since most PIT recipients have not developed the advanced complications of diabetes. Herein, we describe the improvement and stabilization of diabetic neuropathy and retinopathy in 12 PIT recipients. PATIENTS AND METHODS: Between January 1, 2002, and June 30, 2004, there have been 12 patients who have received PIT. Currently, there are eight patients who have sufficient follow-up to assess the progression of diabetic retinopathy and neuropathy. To assess for disease progression, patients were examined by a single ophthalmologist and single neurologist throughout the study period. Eye exams were performed using a slit-lamp exam while neurological status was assessed using electromyelograms and clinical exams. RESULTS: All PIT recipients had decreases in hemoglobin A(1)C and increases in serum C-peptide. All study patients had stabilization of their retinopathic disease. One patient demonstrated improvement of retinopathy at 1 year posttransplant. Fifty percent of patients demonstrated improvement or stabilization of their diabetic neuropathy. One patient had mild reinnervation of the fingers and wrist extensors by clinical exam 1 year posttransplant. Four patients exhibited an average decrease of 19% in sural nerve conduction velocities. CONCLUSION: Our series has demonstrated that all PIT recipients have had stabilization of their diabetic retinopathy and that 50% of patients exhibited stabilization or even improvement of their diabetic neuropathy.

Adult↗
PubMed2002

A preventative foot care programme for people with diabetes with different stages of neuropathy.

The aim of this study was to assess the efficacy of a preventative foot care programme, applied in a normal outpatient setting to decrease the incidence of foot ulcers in people with diabetes diagnosed as having neuropathy by neuropathy disability score (NDS), in relation to the severity of neuropathy based on the vibration perception threshold (VPT). A structured continuous preventative foot care programme was designed to ensure proper footwear, walking foot hygiene, callus care, nailcutting, water temperature checks, use of warming devices, bathroom surgery, foot care products and self-inspection. Continual foot-care education and treatment, including podiatry, were available. Evaluation was at least every 6 months. Diabetic patients (n=308) with neuropathy (NDS > or =6), 72.3+/-10.7 years old, 45% men, 10.9+/-8.8 years duration of diabetes, and HbA(1c) 6.5+/-1.3%, without a history of foot lesions were recruited over 3 years and followed-up for 4.6 (3-6) years. A low risk group (n=124) had a VPT<25 V while 184 had a VPT > or =25 V (high risk). In all 220 patients (71%) complied with the programme, compliance being 76 and 68% in low and high risk groups. The low risk group developed nine ulcers in nine patients, and the high risk group 24 ulcers in 19 patients. Of these eight and 19 ulcers, respectively, were in the non-compliant patient group, giving relative risk of 22 and eight compared with people attending the programme. Thus compliance with a preventative foot programme reduces the incidence of foot ulceration in people with diabetes with neuropathy. This decrease is relatively greater in patients with less severity of neuropathy. The simple design should be widely generalisable.

Diabetic Foot↗
PubMed1988

Microalbuminuria in diabetic subjects with chronic peripheral neuropathy.

Fifty-five patients with chronic peripheral neuropathy, 31 with and 24 without retinopathy, had albumin excretion rates determined on 2-h supine urine collections on three occasions by a radioimmunoassay method. Four patients with retinopathy had albustix-positive proteinuria and were excluded from subsequent analysis. Microalbuminuria was found in 20 of the 27 patients with retinopathy compared with 10 of the 24 patients with neuropathy alone. The mean albumin excretion rate (AER) was higher in neuropathic patients with retinopathy than in those patients with neuropathy alone (41.2 +/- 40.3 vs 18.8 +/- 33.2 micrograms/min, P less than 0.01). Multivariate analysis of the data was performed and this revealed a correlation coefficient of R2 = 0.33 (P less than 0.01) for AER as the dependent variable with respect to the independent variables HbA1, systolic blood pressure and known duration of diabetes. There was, however, no significant contribution separately of these individual variables to the regression equation. Microalbuminuria was significantly associated with retinopathy although almost half of the patients with neuropathy alone had microalbuminuria. The association between microalbuminuria and neuropathy even in the absence of retinopathy provides support for a microvascular element in the pathogenesis of diabetic neuropathy.

Albuminuria↗
PubMed2003

Diabetic neuropathy and nerve regeneration.

Diabetic neuropathy is the most common peripheral neuropathy in western countries. Although every effort has been made to clarify the pathogenic mechanism of diabetic neuropathy, thereby devising its ideal therapeutic drugs, neither convinced hypotheses nor unequivocally effective drugs have been established. In view of the pathologic basis for the treatment of diabetic neuropathy, it is important to enhance nerve regeneration as well as prevent nerve degeneration. Nerve regeneration or sprouting in diabetes may occur not only in the nerve trunk but also in the dermis and around dorsal root ganglion neurons, thereby being implicated in the generation of pain sensation. Thus, inadequate nerve regeneration unequivocally contributes to the pathophysiologic mechanism of diabetic neuropathy. In this context, the research on nerve regeneration in diabetes should be more accelerated. Indeed, nerve regenerative capacity has been shown to be decreased in diabetic patients as well as in diabetic animals. Disturbed nerve regeneration in diabetes has been ascribed at least in part to all or some of decreased levels of neurotrophic factors, decreased expression of their receptors, altered cellular signal pathways and/or abnormal expression of cell adhesion molecules, although the mechanisms of their changes remain almost unclear. In addition to their steady-state changes in diabetes, nerve injury induces injury-specific changes in individual neurotrophic factors, their receptors and their intracellular signal pathways, which are closely linked with altered neuronal function, varying from neuronal survival and neurite extension/nerve regeneration to apoptosis. Although it is essential to clarify those changes for understanding the mechanism of disturbed nerve regeneration in diabetes, very few data are now available. Rationally accepted replacement therapy with neurotrophic factors has not provided any success in treating diabetic neuropathy. Aside from adverse effects of those factors, more rigorous consideration for their delivery system may be needed for any possible success. Although conventional therapeutic drugs like aldose reductase (AR) inhibitors and vasodilators have been shown to enhance nerve regeneration, their efficacy should be strictly evaluated with respect to nerve regenerative capacity. For this purpose, especially clinically, skin biopsy, by which cutaneous nerve pathology including nerve regeneration can be morphometrically evaluated, might be a safe and useful examination.

Animals↗
PubMed2003

Medical evaluation and treatment of diabetic peripheral neuropathy.

Diabetes mellitus is a major health concern that is only expected to become more prevalent over the next few decades. It causes much morbidity and mortality through various macro- and microvascular complications, including diabetic neuropathy. Currently, there is no treatment that directly affects the natural course of diabetic neuropathy except for rigorous glycemic control, a goal that is not always achievable. Despite these therapeutic limitations, the morbidity caused by diabetic neuropathy can be minimized by early and accurate diagnosis. A detailed history and physical examination, along with carefully selected laboratory tests will confirm the presence of diabetic neuropathy while excluding other etiologies that may require alternative management strategies. Treatment is always tailored to the patient's symptoms. In addition to improved glycemic control, health care providers can provide education, support, and symptomatic relief. There are many pain modulating therapies that are effective in diabetic neuropathy as discussed above. Nortriptyline at low doses is an inexpensive well-tolerated medication that is effective. Gabapentin is an excellent choice when nortriptyline is ineffective or not tolerated. Other anticonvulsants, such as lamotrigine, carbamazepine, oxycarbazepine, and topiramate, may also provide benefit. Judicious use of narcotics is appropriate when other treatment modalities fail. The importance of treating underlying depression cannot be overemphasized. When gait becomes impaired as a result of neuropathy, appropriate prescription of assistive devices will prevent injuries from falls. Ankle-foot orthoses and other orthotic devices may allow patients to remain ambulatory and independent for a longer period. Despite the challenges ahead, the future holds the promise of more effective treatments for diabetes mellitus and its complications.

Analgesics↗
PubMed2002

Exclusion of serine palmitoyltransferase long chain base subunit 2 (SPTLC2) as a common cause for hereditary sensory neuropathy.

Recently point mutations in the SPTLC1 subunit of serine palmitoyltransferase have been shown to cause the common form of dominant hereditary sensory neuropathy (HSN1). Serine palmitoyltransferase (SPT) is a heterodimeric molecule made up of two subunits, SPTLC1 and SPTLC2. Twelve index patients from families with presumed genetic sensory neuropathies were screened for SPTLC2 mutations. These families comprised six multigenerational families, including two previously reported families not linked to the SPTLC1 locus on chromosome 9 and one multigenerational family with a complicated hereditary sensory neuropathy syndrome with associated palmar plantar keratosis, ataxia and spastic paraplegia. The remaining families included one consanguineous family with presumed recessive HSN with two affected siblings, one case of congenital sensory neuropathy and four sporadic cases with adult onset sensory neuropathy. No mutations in the SPTLC2 gene were found in any family. These results suggest that SPTLC2 mutations are not a common cause for genetic sensory neuropathies.

Acyltransferases↗
PubMedDate not supplied

Cardiac sympathetic dysinnervation in Type 2 diabetes mellitus with and without ECG-based cardiac autonomic neuropathy.

To evaluate the presence and extent of global and regional distributions of cardiac sympathetic dysinnervation in Type 2 diabetes mellitus I-123-metaiodobenzylguanidine (I-123-MIBG) scintigraphy was applied to 15 Type 2 (noninsulin-dependent) diabetic patients with ECG-based cardiac autonomic neuropathy (> or = two of five age-related cardiac reflex tests abnormal) and 15 clinically comparable Type 2 diabetic patients without ECG-based cardiac autonomic neuropathy. Myocardial perfusion abnormalities were excluded by 99 m-Tc-methoxyisobutylisonitrile (99 m-MIBI) scintigraphy. Both in Type 2 diabetic patients with and without, ECG-based autonomic neuropathy, only one patient (7%) was found to have a normal homogeneous uptake of I-123-MIBG compared to 14 patients (93%) with a reduced I-123-MIBG uptake. The uptake of I-123-MIBG in the posterior myocardium of diabetic patients was smaller than in the anterior, lateral, and septal myocardium (P< .001, P< .001, P< .001, respectively). Diabetic patients with ECG-based cardiac autonomic neuropathy demonstrated a more pronounced reduction of the posterior I-123-MIBG myocardial uptake than diabetic patients without (P< .01). The mean global and the anterior, lateral, septal, and apical myocardial I-123-MIBG uptake was comparable between the two groups. The uptake of the posterior myocardial region correlated with all indices of heart rate variation at rest and during deep breathing. A correlation between global or regional myocardial I-123-MIBG uptake and QT interval was not observed. The study demonstrates that cardiac sympathetic dysinnervation is common in Type 2 diabetes mellitus both with and without ECG-based cardiac autonomic neuropathy. In Type 2 diabetes mellitus, the posterior myocardium is predominantly affected and the extent of dysinnervation is more pronounced in the presence of ECG-based cardiac autonomic neuropathy.

3-Iodobenzylguanidine↗
PubMedDate not supplied

No correlation between impairment of cerebrovascular reserve capacity and electrophysiologically assessed severity of neuropathy in noninsulin-dependent diabetes mellitus.

INTRODUCTION: Microvascular abnormalities have an important role in the most frequent neurological complications of diabetes mellitus: neuropathy and cerebrovascular disorders. Severity of neuropathy as well as of cerebral microvascular damage can be quantitatively evaluated by instrumental methods like nerve conduction studies and transcranial Doppler. In the present study, we investigated whether a correlation exists between the severity of peripheral neuropathy and the impairment of cerebrovascular reserve capacity (CRC) in 20 patients with Type 2 diabetes mellitus. METHODS: CRC was measured by transcranial Doppler and defined as the maximal percentage increase in blood flow velocity in the middle cerebral artery within 20 min after an intravenous dose of 1000 mg of acetazolamide. Nerve conduction studies of the median, ulnar, peroneal, and sural nerves were performed. Severity of neuropathy was scored based on conduction velocities, amplitudes, and distal latencies. RESULTS: There was no correlation between the neuropathic score and CRC (R= .003, P= .99). Neither CRC nor the neuropathic score correlated significantly with age, duration of diabetes, and serum values of HbA(1c), glucose, insulin, von Willebrand factor, and alpha(2) - macroglobulin. Severity of neuropathy but not CRC correlated with microalbuminuria (R= .47, P= .038 and R= .14, P= .54). Improper treatment reflected by HbA(1c) >10% was associated with significantly more severe albuminuria, higher actual blood glucose level, higher von Willebrand factor activity, and marginally higher neuropathic score (21 vs. 13, P=.096), but was not associated with CRC (44% vs. 42%, P= .81). When duration of diabetes was dichotomized to 15 years and less or over 15 years, CRC was significantly smaller (35% vs. 50%, P= .036) and neuropathy was more severe in the subgroup with longer diabetes duration (19 vs. 11.5 points, P= .07). CONCLUSIONS: Although both CRC and peripheral nerve function are affected more severely in patients with long-lasting Type 2 diabetes mellitus, damage in the cerebrovascular system and in the long peripheral nerves occur independently. As in diabetes mellitus pathological changes in autonomic and large peripheral nerves develop simultaneously, decreased CRC in diabetic patients might be predominantly due to structural changes of resistance arteries or to metabolic than to neurogenic factors.

Adult↗
PubMed1987

Loss of spontaneous variability of fingertip anastomotic blood flow in diabetic autonomic neuropathy.

We have employed a thermal clearance probe to study fingertip blood flow, which comprises predominantly arteriovenous anastomotic flow. In non-diabetic subjects there was a marked variability in resting fingertip blood flow which was of similar magnitude to that in diabetic subjects without autonomic neuropathy. In 20 diabetic subjects with increasing severity of autonomic neuropathy there was a reduction of spontaneous variability in flow (r = 0.59, P less than 0.001), which was not related to differences in basal flow, in skin thickness or in age. There was no relationship between maximal flow and severity of autonomic neuropathy (r = 0.08), although basal flow was decreased in subjects with moderate, but not those with severe, autonomic neuropathy (P less than 0.01 and P less than .04 compared with controls). Our failure to find an increase in basal fingertip flow in autonomic neuropathy could imply that spontaneous variability of anastomic flow is lost before increased arteriovenous shunting becomes apparent, but it could result from the indirect heating employed in the study causing vasodilatation in subjects without neuropathy.

Adult↗
PubMed2002

The relationship between blood glucose excursions and painful diabetic peripheral neuropathy: a pilot study.

AIMS: Peripheral neuropathy affects 30% of Type 1 diabetic patients. Unfortunately, 10-20% of affected patients have disabling symptoms. The aim of this study was to examine the relationship between blood glucose excursions and pain in patients with symptomatic diabetic neuropathy. METHODS: Twenty Type 1 diabetic patients with peripheral neuropathy (10 painful and 10 painless) wore a continuous glucose monitoring system for 3 days. Symptomatic patients kept a daily pain score diary. The mean amplitude of glycaemic excursions (MAGE) and the M-values (measure of glucose deviations from an arbitrarily selected point) were calculated. RESULTS: Groups were matched for (mean +/- sd) age: 52.0 +/- 11.1 years; duration of diabetes: 24.8 +/- 10.7 years; HbA1c: 9.7 +/- 2.3%; duration of neuropathy: 5.6 +/- 2.6 years; and CGMS performance. The painful group had a greater mean glucose (12.1 +/- 2.9 mmol/l vs. 9.3 +/- 1.9 mmol/l, P = 0.02), a greater M-value (68.4 vs. 31.1, P = 0.02) and more glycaemic excursions (13 vs. 10, P < 0.01), compared with the painless group. However, there was no difference in the MAGE between both groups, and no correlation between the number of glycaemic excursions and the number of painful episodes in the painful group. CONCLUSIONS: Patients with painful neuropathy have greater glucose flux and possibly poorer diabetes control, compared with patients with painless neuropathy.

Adult↗
PubMed2000

Gene expression of antioxidant enzymes in experimental diabetic neuropathy.

Chronic hyperglycemia results in a large deficit in nerve blood flow. Both autoxidative- and ischemia-induced lipid peroxidation occurs, with resultant peripheral sensory neuropathy in streptozotocin-induced diabetes in the rat. Free radical defenses, especially involving antioxidant enzymes, have been suggested to be reduced, but scant information is available on chronic hyperglycemia. We evaluated the gene expression of glutathione peroxidase, catalase, and superoxide dismutase (cuprozinc and manganese separately) in L4,5 dorsal root ganglion (DRG) and superior cervical ganglion, as well as enzyme activity of glutathione peroxidase in DRG and sciatic nerve in experimental diabetic neuropathy of 3 months and 12 months durations. We also evaluated nerve electrophysiology of caudal, sciatic-tibial, and digital nerves. A nerve conduction deficit was seen in all nerves in experimental diabetic neuropathy at both 3 and 12 months. Gene expression of glutathione peroxidase, catalase, cuprozinc superoxide dismutase, and manganese superoxide dismutase were not reduced in experimental diabetic neuropathy at either 3 or 12 months. Catalase mRNA was significantly increased in experimental diabetic neuropathy at 12 months. Glutathione peroxidase enzyme activity was normal in sciatic nerve. We conclude that gene expression is not reduced in peripheral nerve tissues in very chronic experimental diabetic neuropathy. Changes in enzyme activity may be related to duration of diabetes or due to post-translational modifications.

Animals↗
PubMed2003

Demyelinating focal motor neuropathy of the ulnar nerve masquerading as compression in Guyon's canal: a case report.

Ulnar nerve-innervated intrinsic muscle weakness, in the absence of sensory complaints or deficits, usually is the result of compression at the ulnar nerve in zone II of Guyon's canal. In rare instances the problem is not caused by a compressive neuropathy but by a demyelinating focal motor neuropathy. Demyelinating neuropathies have been well documented in the neurologic literature but they have received little attention in the hand surgery literature. We report on one such case and the importance of differentiating the 2 neuropathies. Although surgery often is necessary for a compressive neuropathy it is contraindicated for a demyelinating neuropathy.

Adult↗
PubMed2001

The natural history of diabetic peripheral neuropathy determined by a 12 year prospective study using vibration perception thresholds.

The development and long term progression of diabetic peripheral neuropathy was studied using vibration perception threshold (VPT) as a validated measure. Three hundred and ninety-two patients had a normal age corrected VPT (12.1 +/- 3.7 volts) at baseline, with an age corrected logarithmic VPTscore < 12. 19.9% developed an abnormal VPT over a 12 year period, increasing from 14.2 +/- 3.7 volts (VPTscore 10.4 +/- 0.6) at baseline to 35.9 +/- 9.5 volts (VPTscore 12.6 +/- 0.45) at follow up (P = 0.0001), and from 10.1 +/- 3.7volts (VPTscore 9.4 +/- 0.8) to 14.2 +/- 4.7 (VPTscore 9.8 +/- 0.8) in the rest. Over 80% thus retained a "normal" VPT after a mean diabetes duration of 16 years despite only average glycaemic control, suggesting that non-ideal long term glycaemic control leads to neuropathy in a subset of predisposed patients. VPT was correlated in 123 diabetic patients with definitive criteria for neuropathy and a range of quantitative sensory and autonomic tests. 62/63 patients with abnormal VPT fulfilled neuropathy criteria; of patients with normal VPT who fulfilled neuropathy criteria, all had at least one abnormal thermal threshold test result. We conclude that a combination of log-transformed VPT values (VPTscore > 10.1) and thermal thresholds can identify diabetic patients at risk of developing peripheral neuropathy and select patients likely to benefit from prophylaxis in clinical trials.

Adult↗
PubMed2004

Posterior ischemic optic neuropathy: case report of a rare complication after general surgery.

BACKGROUND: Posterior ischemic optic neuropathy (PION) is a rare cause of bilateral severe and bilateral visual loss. Three mechanisms for posterior ischemic optic neuropathy are recognized: arteritic, non-arteritic, and peri- or postoperative. We report a case of bilateral postoperative posterior ischemic optic neuropathy. HISTORY AND SIGNS: A previously healthy 51-year-old man complained of the sudden onset of visual loss and unformed visual hallucinations in both eyes, 24 hours after an uneventful lumbar spine surgery. Duration of surgery was 12 hours with 2.5 liters of blood loss. At the time of visual loss, anemia was 74 g/L. Ophthalmic examination revealed decreased visual acuity to count fingers and normal optic disc without swelling or hemorrhages in both eyes. THERAPY AND OUTCOME: Despite blood transfusion 2 days after visual loss, evolution was stable. One month later, visual acuity was 0.15 RE and 0.2 LE with severe dyschromatopsia. Pupils reacted sluggishly to light but briskly to convergence. Optic discs were diffusely pale. DISCUSSION: Peri- and postoperative posterior ischemic optic neuropathy is a rare but devastating complication of surgery performed at distance from the visual pathways and its vascularization. Risk factors include: spine surgery, peri-operative hypotension, anemia, facial edema. Early recognition of posterior ischemic optic neuropathy and rapid correction of hypotension and/or anemia might improve outcome of posterior ischemic optic neuropathy, which usually is poor.

Anemia↗
PubMed1984

Decreased response of epinephrine and norepinephrine to insulin-induced hypoglycemia in diabetic autonomic neuropathy.

The responses of epinephrine, norepinephrine and other counter-regulatory hormones to insulin-induced hypoglycemia were investigated in 5 diabetics who showed signs of autonomic neuropathy, in 7 age-matched diabetics without autonomic neuropathy and in 7 healthy subjects. The presence of autonomic neuropathy was evaluated by decreased beat-to-beat variation in heat rates during hyperventilation or orthostatic hypotension. Catecholamines were determined by a totally automated plasma catecholamine analyzing system using a two-column system of high performance liquid chromatography. Plasma epinephrine and norepinephrine responses to hypoglycemia in diabetics with autonomic neuropathy were significantly lower than those in diabetics without autonomic neuropathy. Plasma glucagon response in diabetics was apparently attenuated compared to normal controls and there was no significant difference in glucagon response between the two patient groups. Other counter-regulatory hormone responses did not differ among the three groups. The data demonstrate that the responses of plasma epinephrine and norepinephrine to insulin-induced hypoglycemia are impaired in diabetics with autonomic neuropathy.

Adult↗
PubMed2000

Oral symptoms and signs in elderly patients with type 2 diabetes mellitus. A focus on diabetic neuropathy.

OBJECTIVE: We investigated oral disorders and compared the findings with the occurrence of neuropathy in type 2 diabetes mellitus. STUDY DESIGN: Mucosal diseases, tooth loss, and temporomandibular joint dysfunction were examined in 45 patients with long-term type 2 diabetes mellitus and in 77 control subjects. The occurrence of neuropathy was evaluated by neurophysiologic tests. RESULTS: Of patients with diabetes, 56% suffered from dry mouth and 18% from glossodynia; of controls, correspondingly, 36% and 7% (P <.05); 2 or more mucosal lesions were detected in 42% and 20%, respectively (P =. 008). Temporomandibular joint dysfunction was found in 27% of subjects with diabetes and in 16% of control subjects. Peripheral neuropathy was present in 42% of patients with diabetes and in none of the controls (P <.01), and autonomic parasympathetic neuropathy in 54% and 31%, respectively (P =.02). Peripheral and autonomic parasympathetic neuropathies were independent risk factors for tooth loss and temporomandibular dysfunction. CONCLUSIONS: Diabetic neuropathy was found to be associated with tooth loss and temporomandibular joint dysfunction.

Age Factors↗
PubMed1988

Increase in albumin, IgG, and IgM blood-nerve barrier indices in human diabetic neuropathy.

The albumin (Alb), IgG, and IgM concentrations in the endoneurium of fascicular sural nerve biopsy samples were evaluated in controls (n = 9 or 10), diabetic patients without neuropathy (n = 6), and diabetic patients with polyneuropathy (n = 17 or 18). These values were significantly increased in diabetic patients with and without neuropathy when expressed both per endoneurial dry weight or endoneurial total protein compared to biopsy samples from healthy controls. When these concentrations, expressed per endoneurial total protein, were related to plasma concentrations similarly expressed, the resulting blood-nerve barrier (BNB) indices were significantly increased for Alb (6.1 times; P less than 0.00001), IgG (4.9 times; P = 0.00037), and IgM (2.7 times; P = 0.015). The diabetic patients without neuropathy (defined as having an index of pathology of greater than 0.65; a measure of the severity of the pathological abnormality based on morphological criteria) also had significant increases in two of these BNB indices that were intermediate between the diabetic neuropathy patients and controls (Alb, 3.9 times controls; P = 0.00002: IgG, 4.6 times controls; P = 0.00016: IgM, 1.8 times controls; not significant). No correlations were observed between the endoneurial concentrations of these plasma proteins or the BNB indices and the index of pathology, suggesting that these increases in endoneurial plasma proteins precede the pathologic alterations. The increased values for the diabetics in the absence of pathological abnormalities may prove useful in predicting neuropathic complications. The ratio of the IgG-BNB index to the Alb-BNB index was decreased 19%, and the ratio of the IgM-BNB index to the Alb-BNB index was decreased 56% in diabetic neuropathy patients compared to controls. Although the IgG and IgM concentrations are increased in the diabetic endoneurium, the Alb increase is greater and a mechanism other than size indiscriminate extravasation of plasma proteins, therefore, is suggested. Morphometric assessment of the endoneurial compartments, which would be expected to contain these plasma proteins, suggests that they are not altered in diabetic neuropathy; hence, it is hypothesized that the observed increase in endoneurial concentration of these plasma proteins results from altered transport through the endothelial or perineurial barrier, which supports an underlying vascular mechanism in the development of diabetic polyneuropathy.

Adult↗
PubMed1998

Neuropathy in non-insulin-dependent diabetes mellitus. The significance of symptoms.

OBJECTIVE: Clinical evaluation of significance of symptoms suggestive of neuropathy in non-insulin-dependent diabetics in general practice. DESIGN: Case control study. Interviewer-administered questionnaire. Physical examination by general practitioner researcher. SETTING: Government family practice clinic in Singapore. SUBJECTS: 55 patients with non-insulin-dependent diabetes (NIDDM) aged 35-84 years (51% males), and 53 non-diabetic controls matched for age (+/- 5 years) and gender. MAIN OUTCOME MEASURES: Proportions of subjects with presence of symptoms and physical signs. RESULTS: More patients than controls experienced symptoms suggestive of distal neuropathy (paraesthesiae: 13 vs. 4%), and lower extremity proximal myopathy (weakness climbing stairs: 42 vs. 19%, getting up from squatting position: 31 vs. 11%). No difference in proportions of patients and controls experiencing symptoms suggestive of autonomic neuropathy. More patients than controls had absent tendon reflexes (35 vs. 13%) and weaker hip muscles (24 vs. 6%). Of all who experienced symptoms indicating peripheral neuropathy, 36% of patients had absent tendon reflexes, compared with 8% of controls; and of those who experienced weakness of hip muscles, 31% of patients and 12% of controls had diminished power in the hip muscles. CONCLUSION: Symptoms suggestive of diabetic neuropathy are common and should be asked about in the routine follow-up of patients with diabetes. Up to a third of patients with symptoms will have clinical signs of diabetic neuropathy.

Adult↗