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PubMed2003

Increased sural nerve epineurial blood flow in human subjects with painful diabetic neuropathy.

AIMS/HYPOTHESIS: The pathogenesis of painful diabetic neuropathy remains unknown. As a consequence we still do not have any effective, rational treatments and a greater understanding of the mechanisms is urgently required. Previous studies have shown no consistent morphological differences in the nerves of patients with and without painful neuropathy. The aim of this study was to compare epineurial haemodynamics in patients with chronic painful and painless neuropathy. METHODS: The techniques of microlightguide spectrophotometry and fluorescein angiography were used to measure epineurial intravascular oxygen saturation and blood flow respectively. Eleven patients with painful and eight with painless neuropathy were studied, with the groups matched carefully in terms of severity of neuropathy and diabetes control. RESULTS: Intravascular oxygen saturation was higher in the painful neuropathy group compared to those without pain (median 73.8% vs 67.7%, respectively; p=0.021). Fluorescein rise time was also faster in those with painful symptoms (median 18.3 s vs 53.6 s; p=0.046) indicating higher epineurial blood flow in these subjects. CONCLUSION/INTERPRETATION: These results indicate that there are distinct differences in haemodynamics within the epineurium of the sural nerve in subjects with painful and painless neuropathy. Haemodynamic factors could therefore have an important role in the pathogenesis of neuropathic pain and might offer further insight into potential treatments for this distressing condition.

Blood Flow Velocity↗
PubMed1999

A new minimally invasive technique to show nerve ischaemia in diabetic neuropathy.

AIMS/HYPOTHESIS: Experimental studies have shown that abnormalities of nerve microcirculation are important factors in the pathogenesis of diabetic neuropathy but there have been few clinical studies. We have applied microlightguide spectrophotometry to measure intravascular oxygen saturation (HbO2%) and blood flow in human sural nerve. METHODS: We studied ten patients with mild-moderate sensory motor diabetic neuropathy, nine patients without neuropathy and nine control subjects. We took 300 measurements of oxygen saturation under direct visual control through a 1.9 mm rigid endoscope over three regions of the nerve. Spectrophotometric measurements of nerve fluorescence were taken after an intravenous injection of sodium fluorescein and the rate of increase in nerve fluorescence (rise time) was used as an indicator of nerve blood flow. RESULTS: Nerve oxygen saturation was reduced in patients with neuropathy compared with control subjects (67.1 +/- 2.2% vs 76.7 +/- 2.1%, p = 0.006). Fluorescein rise time was prolonged in patients with neuropathy compared with the control group (48.5 +/- 7.0 s vs 14.0 +/- 3.1 s, p = 0.001) suggesting impaired nerve blood flow. There was a correlation between rise time, nerve oxygen saturation, glycaemic control and sural nerve sensory conduction velocity (p < 0.01). CONCLUSION/INTERPRETATION: The combination of microlight-guide spectrophotometry and micro-endoscopy provides a valuable minimally invasive technique for clinical investigation of nerve microcirculation. We have shown reduced nerve oxygenation and impaired blood flow in diabetic neuropathy and these findings strongly support a central role of microvascular disease in the pathogenesis of diabetic neuropathy.

Diabetic Neuropathies↗
PubMed1999

Experimental diabetic neuropathy: an update.

Diabetic neuropathy consists of several clinical syndromes affecting motor, sensory and autonomic nerves. Of these the most common is distal symmetric sensory polyneuropathy usually referred to as diabetic neuropathy. Animal studies, mainly in diabetic rodents, have contributed tremendously to our understanding of this disease. From these it is clear that the pathogenesis of diabetic neuropathy is multifactorial involving sequentially occurring and often closely interrelated metabolic aberrations. Major pathogenetic mechanisms include increased activity of the polyol pathway, abnormalities in vasoactive substances, non-enzymatic glycation, increased presence of free radicals, and perturbed neurotrophism. Traditionally the neuropathies accompanying Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus have been regarded as identical. Recent investigations have, however, clearly delineated distinct differences in the functional and structural expressions of the neuropathies in the two types of diabetes. Major future challenges are the identification of the differences in underlying pathogenetic mechanisms in the two types of neuropathy and in gaining a better understanding of the hierarchy of the multifactorial mechanisms underlying the disease. This will be important for designing meaningful therapies which to date have failed miserably in diabetic neuropathy.

Animals↗
PubMed1999

Correlation of acetylator phenotype with peripheral, autonomic and central neuropathy in Northern Indian non-insulin-dependent diabetes mellitus patients.

OBJECTIVES: Genetic susceptibility to diabetic neuropathy has been suspected and tentatively explored; however, diabetic autonomic and central neuropathies are poorly investigated areas. Previous trials correlating types of diabetes and diabetic neuropathy with acetylator dimorphisms have not been conclusive. The present study was designed to test peripheral neuropathy, autonomic neuropathy and integrity of central conduction pathways in patients of non-insulin-dependent diabetes mellitus (NIDDM), and to correlate the findings with the acetylator phenotype. METHODS: Twenty-six patients of NIDDM with stable glycaemic control and 11 age- and sex-matched control subjects were recruited, clinically examined and investigated with glycaemic and lipid profile, renal function tests, nerve conduction studies (sensory and motor), auditory brain stem evoked responses (ABERs) and somatosensory evoked potentials (SEPs). Acetylator status of the subjects was determined by sulphadimidine test. RESULTS: Out of 26 NIDDM patients, eight (30.7%; group 1A) were slow acetylators and 18 (69.3%; group 1B) were fast acetylators. The distribution of slow and rapid acetylators in both the groups was similar. Glycaemic and lipid profiles and 24-h urinary albumin excretion in groups 1A and 1B were also similar. Motor nerve conduction velocity, latency of F wave, sensory nerve conduction and amplitudes of sensory nerve action potentials were not different between fast and slow acetylator NIDDM patients. On testing for ABERs, there were no statistically significant differences in peak latencies of waves I, III and V; interpeak latencies (IPLs) I-III, III-V and I-V; amplitude of waves I, III and V on both sides between NIDDM patients and controls. However, peak latencies of wave III (P < 0.01), wave V (P < 0.005), IPLs I-III and I-V (P < 0.005), IPLs III-V (P < 0.05), and amplitudes of wave I (P < 0.05) and wave V (P < 0.05) on the left side were significantly different in slow acetylator NIDDM patients. Increase on the right side for the same group was statistically significant for IPLs I-III and I-V (P < 0.05). SEPs showed no statistically significant difference between NIDDM patients and controls, and slow and fast acetylator NIDDM patients. CONCLUSIONS: No significant association of acetylator status with peripheral neuropathy in NIDDM subjects was observed in the present study. However, central neural conduction, primarily tested by ABERs, was significantly delayed in slow acetylators compared with fast acetylator NIDDM patients. Hence, there may be a predisposition to neuropathy in this group of patients, and such a predisposition may be better detected by studying central rather than peripheral nervous conduction pathways in NIDDM patients.

Adult↗
PubMed1998

Reactive, degenerative, and proliferative Schwann cell responses in experimental galactose and human diabetic neuropathy.

Despite early descriptions of hypertrophic Schwann cells and onion-bulb formation in patients with diabetic neuropathy, clinical and experimental studies have emphasized axonal pathology. In recent years, the Schwann cell has been further implicated in diabetic neuropathy because it is the primary intrafascicular location for the first enzyme of the polyol pathway, aldose reductase, which appears to have a role in modulating a variety of complications of diabetes, including diabetic neuropathy. To further explore the role of polyol pathway flux in the pathogenesis of Schwann cell injury, ultrastructural abnormalities of Schwann cells in human diabetic neuropathy (HDN) were compared with those in experimental galactose neuropathy (EGN), a well-characterized model of hyperglycemia without hypoinsulinemia. Similar to previous studies of EGN, reactive, degenerative and proliferative changes of Schwann cells were observed after 2, 4 and 24 months of galactose intoxication. Reactive changes included accumulation of lipid droplets, pi granules of Reich and glycogen granules, increased numbers of subplasmalemmal vesicles, cytoplasmic expansion, and capping. Degenerative changes included enlargement of mitochondria and effacement of cristae, and disintegration of both abaxonal and adaxonal cytosol and organelles. Both demyelination and onion-bulb formation were seen at all time points, although supernumerary Schwann cells and axonal degeneration were most numerous after 24 months of galactose feeding. In sural nerve biopsy samples from patients with diabetes and progressive worsening of neuropathy, ultrastructural abnormalities in Schwann cells encompassed the full range of reactive, degenerative and proliferative changes described in galactose-fed rats. The concordance of fine-structural observations in nerves from galactose-fed rats and these adult-onset diabetic patients emphasizes the role of flux through aldose reductase in the complex pathology of diabetic neuropathy and points to the utility of galactose intoxication in helping to understand this metabolic disorder.

Adult↗
PubMed2003

Diagnosis of hereditary neuropathies in adult patients.

This paper reviews the clinical diagnostic approach to hereditary neuropathies in adults by analysing: elements that point to a neuropathy of inherited origin, different modalities of presentation, laboratory and instrumental diagnostic tests, including molecular tests, symptoms and signs of involvement of other organs. Different phenotypes may be identified according to: disease course; involvement of motor, sensory, autonomic fibres; site of lesion (neuropathy versus neuronopathy); calibre of involved fibres (small-fibre versus large-fibre neuropathy); presence of distinctive symptoms (neuropathic pain); involvement of other organs or apparatus. Charcot-Marie-Tooth disease, Familial Amyloid Polyneuropathy, Hereditary Sensory and Autonomic Neuropathy, Fabry disease, Tangier disease, Porphyric Neuropathies, Refsum disease, Hereditary Neuropathy with liability to Pressure Palsies, Hereditary Neuralgic Amyotrophy, and other rare disorders involving the peripheral nervous system are reviewed.

Acute Disease↗
PubMed1998

Uncommon early-onset neuropathy in diabetic patients.

An acute neuropathy rarely occurs early in the course of diabetes mellitus. Five cases are described of adult patients who developed a peripheral neuropathy at the time or shortly after the onset or discovery of diabetes mellitus. Patient 1, an 80-year-old woman who developed a subacute tetraparesis with proximal and distal muscle weakness with normal cranial nerves, proved to have insulin-requiring diabetes mellitus. In the other patients, all men aged 23-34 years, symptomatic neuropathy occurred simultaneously (patient 2) or 1-6 months after the onset of insulin-dependent diabetes mellitus (IDDM) (patients 3-5). Patients 2 and 3 developed a symptomatic multifocal neuropathy; patients 4 and 5, a painful distal symmetrical sensory polyneuropathy (DSSP) shortly after beginning treatment with insulin. Nerve biopsy showed active axonal lesions in patients 2 and 5 and mixed axonal and demyelinating lesions in the others, with severe axon loss in patients 4 and 5. Vasculitic lesions were found in patient 2, who improved without additional treatment. Neurological examination remained unchanged after 2 years in patients 3-5. Although a coincidence cannot be excluded for patients 1-3, whose neuropathy was not of the pattern commonly found in diabetes, it is suggested that acute disequilibrium in the diabetic status may facilitate the occurrence of a variety of neuropathies. Alternatively, the autoimmune process which led to IDDM may also trigger an autoimmune neuropathy with vasculitis (patient 2) or demyelinative nerve lesions. Only the distal symmetrical sensory polyneuropathy with severe axonal lesions observed in patients 4 and 5 seems directly related to diabetes mellitus. In spite of their occurrence shortly after beginning insulin therapy, the role of treatment with insulin in the onset is uncertain.

Acute Disease↗
PubMed1998

Prognosis of patients with primary systemic amyloidosis who present with dominant neuropathy.

BACKGROUND: Primary systemic amyloidosis is an uncommon disorder associated with the desposition of fragments of immunoglobulin light chains in a variety of tissues. Some patients present with peripheral neuropathy. The prognosis of these patients is not clear. METHODS: We searched the medical records of all patients seen at the Mayo Clinic between January 1, 1978 and December 31, 1994 with the diagnosis of amyloidosis. Twenty-six patients with sural nerve biopsy-proven amyloid neuropathy and a documented monoclonal protein in the serum or urine were studied. RESULTS: The most common symptoms that led to the diagnosis of primary amyloid neuropathy were paresthesias (81%), muscle weakness (65%), and numbness (58%). The median duration of symptoms before diagnosis was 29 months. Symptoms of autonomic neuropathy were present at diagnosis in 17 patients (65%). Other organs were involved in most patients. The monoclonal light chain protein detected was lambda in 18 patients (69%) and kappa in 8 (31%). The neuropathy was chronic, debilitating, and showed relentless progression. Twenty-two patients (85%) died (median survival 25 months) and 4 patients were alive at a median follow-up of 4.5 years. Progressive amyloidosis was the cause of death in most patients. Survival was significantly better in the patients with a serum albumin level >3 g/dL (median survival 31 months compared with 18 months; P <0.01, log-rank test). CONCLUSIONS: Patients with primary systemic amyloidosis in whom neuropathy is the dominant clinical manifestation often do not receive a diagnosis until years after the onset of symptoms. The prognosis is worse than previously indicated. Neuropathy does not improve with therapy.

Actuarial Analysis↗
PubMed1997

Aspirin therapy in nonarteritic anterior ischemic optic neuropathy.

PURPOSE: To determine the benefit of aspirin in reducing the risk of nonarteritic anterior ischemic optic neuropathy in the fellow eye following its occurrence in the first eye. METHODS: A retrospective cohort study was conducted on 431 patients, 153 of whom were and 278 of whom were not prescribed aspirin following the development of unilateral nonarteritic anterior ischemic optic neuropathy. RESULTS: The 2-year cumulative probability of nonarteritic anterior ischemic optic neuropathy in the fellow eye was 7% in the aspirin group and 15% in the no-aspirin group, and 5-year cumulative probabilities were 17% and 20%, respectively. Compared with the no-aspirin group, the rate ratio for nonarteritic anterior ischemic optic neuropathy in the fellow eye in the aspirin-user group was 0.43 (95% confidence interval, 0.19 to 0.92) over the first 2 years and 0.68 (95% confidence interval, 0.36 to 1.26) over the 5-year period. The overall calculated 5-year risk was 19%; however, if none of the patients with incomplete follow-up developed nonarteritic anterior ischemic optic neuropathy in the fellow eye, then the 5-year risk would be about 12%. CONCLUSIONS: The 5-year risk of nonarteritic anterior ischemic optic neuropathy occurring in the second eye is far lower than that reported by previous studies. Our results suggest a possible short-term but little or no long-term benefit to aspirin in reducing the risk of nonarteritic anterior ischemic optic neuropathy in the fellow eye. However, this finding must be viewed with caution because this study was not conducted prospectively with a controlled protocol.

Aspirin↗
PubMedDate not supplied

Effect of hyperbaric oxygen on ophthalmic artery blood velocity in patients with diabetic neuropathy.

To assess the relationship between blood flow and the complications of diabetes mellitus, we investigated the changes in the velocity of blood flow in the ophthalmic artery before and after hyperbaric oxygen therapy (HBO), one of the treatments for diabetic neuropathy. Color Doppler imaging was used before and after HBO. Seven diabetic neuropathy patients, 3 diabetics without neuropathy, and 7 normal, control subjects were enrolled. The patients were subjected to breathing 100% oxygen at 2.0 atmosphere absolute (ATA) for 1 hour. Hyperbaric oxygen therapy resulted in an average decrease in blood velocity by 15.0 +/- 9.0% (mean +/- SD) in normal subjects and 10.7 +/- 8.6% in diabetics without neuropathy. Blood velocity returned to the baseline level 4 hours after discontinuation of HBO. In contrast, blood velocity increased by 20.6 +/- 9.5% in diabetic patients with neuropathy irregardless of the severity of the diabetic retinopathy. The resistance index of the ophthalmic artery was not changed during HBO in the group with diabetic neuropathy, indicating that other mechanisms may be implicated, leading to the compensatory changes of blood flow. These results suggest that the increase in the blood velocity in the ophthalmic artery after HBO in diabetic neuropathy patients could be attributed to an imbalance in autonomic nervous function.

Autonomic Nervous System↗
PubMed2002

Clinical trials for drugs against diabetic neuropathy: can we combine scientific needs with clinical practicalities?

Diabetic neuropathy is a chronic progressive disease accounting for considerable morbidity and reduced quality of life among patients with diabetes. Accumulating evidence suggests that the clinical and neurophysiological markers used to assess neuropathy not only predict the development of neuropathic foot ulceration, one of the most common causes for hospital admission and lower limb amputations, but are also predictors of increased mortality in diabetic patients. In addition to metabolic control, drug treatment of both incipient and clinically manifest diabetic neuropathy will be necessary for the years to come. Because 1-2% of the whole population in western societies may be affected, the search for effective drug treatment is not only a very important goal for the patient suffering from diabetic neuropathy and for the practicing physician, but also an economic task for both the health care systems and pharmaceutical companies. The validity of inferences about the clinical consequences of the use of any given agent to induce a specific pharmacologic effect will depend not only on the extent to which it affects the targeted biological phenomenon, but also on the extent to which all of the actions of the agent have been defined and the extent to which all affect the entire organism, alone and in concert. The ultimate test of the usefulness of a drug or device depends on the determination of outcomes, ideally in randomized clinical trials (RCTs) of sufficient scope and duration. The efficacy and safety of a variety of drugs based on the different pathogenetic hypotheses proposed have been evaluated in RCTs since the 1970s. However, the quality of RCTs published between 1981 and 1992 that evaluated the effects of medical treatment in diabetic polneuropathy was poor. Adequate designs for RCTs in diabetic neuropathy must consider the following criteria: type and stage of neuropathy, homogeneity of the study population, outcome measures (neurophysiological markers, intermediate clinical end points, ultimate clinical outcomes, quality of life), natural history, sample size, study duration, reproducibility of neurophysiological and intermediate end points, nonspecific effects of treatment, measures of treatment effect, the extent to which the overall trail result applies to individual patients (external validity), and the reporting of the RCTs. Trials focusing preferentially on patients with mild or moderate early stages of neuropathy over long periods of 3-5 years aimed at slowing or prevention, rather than reversal, using end point measures that have clinical and prognostic significance are most likely to produce meaningful results.

Animals↗
PubMed2004

Neurotrophic factors and their receptors in human sensory neuropathies.

Neurotrophic factors may play key roles in pathophysiological mechanisms of human neuropathies. Nerve growth factor (NGF) is trophic to small-diameter sensory fibers and regulates nociception. This review focuses on sensory dysfunction and the potential of neurotrophic treatments. Genetic neuropathy. Mutations of the NGF high-affinity receptor tyrosine kinase A (Trk A) have been found in congenital insensitivity to pain and anhidrosis; these are likely to be partial loss-of-function mutations, as axon-reflex vasodilatation and sweating can be elicited albeit reduced, suggesting rhNGF could restore nociception in some patients. Leprous neuropathy. Decreased NGF in leprosy skin may explain cutaneous hypoalgesia even with inflammation and rhNGF may restore sensation, as spared nerve fibers show Trk A-staining. Diabetic neuropathy. NGF is depleted in early human diabetic neuropathy skin, in correlation with dysfunction of nociceptor fibers. We proposed rhNGF prophylaxis may prevent diabetic foot ulceration. Clinical trials have been disappointed, probably related to difficulty delivering adequate doses and need for multiple trophic factors. NGF and glial cell line-derived neurotrophic factor (GDNF) are both produced by basal keratinocytes and neurotrophin (NT-3) by suprabasal keratinocytes: relative mRNA expression was significantly lower in early diabetic neuropathy skin compared to controls, for NGF (P < 0.02), BDNF (P < 0.05), NT-3 (P < 0.05), GDNF (< 0.02), but not NT4/5, Trk A or p75 neurotrophin receptor (all P > 0.05). Posttranslational modifications of mature and pro-NGF may also affect bioactivity and immunoreactivity. A 53 kD band that could correspond to a prepro-NGF-like molecule was reduced in diabetic skin. Traumatic neuropathy and pain. While NGF levels are acutely reduced in injured nerve trunks, neuropathic patients with chronic skin hyperalgesia and allodynia show marked local increases of NGF levels; here anti-NGF agents may provide analgesia. Physiological combinations of NGF, NT-3 and GDNF, to mimic a 'surrogate target organ', may provide a novel 'homeostatic' approach to prevent the development and ameliorate intractable neuropathic pain (e.g., at painful amputation stumps).

Animals↗
PubMedDate not supplied

Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial.

BACKGROUND: Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy. METHODS: We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity. FINDINGS: We found no significant difference at baseline for age, HbA1c, blood pressure, or severity of neuropathy between two groups. There was no change in HbA1c over the treatment period. Peroneal motor nerve conduction velocity (p=0.03) and M-wave amplitude (p=0.03) increased, and the F-wave latency (p=0.03) decreased and sural nerve action potential amplitude increased (p=0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group. INTERPRETATION: The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.

Adult↗
PubMed2000

Characterisation of autoantibodies to peripheral myelin protein 22 in patients with hereditary and acquired neuropathies.

To investigate the possibility that an autoimmune mechanism may play a role in the hereditary neuropathy Charcot-Marie-Tooth type 1A (CMT1A), sera were analysed by Western blot for anti-peripheral myelin protein 22 (PMP22) autoantibodies. These sera were compared with sera from patients with CMT type 2 (CMT2), acquired peripheral neuropathies such as chronic inflammatory demyelinating neuropathy (CIDP), anti-MAG IgM neuropathy, Miller-Fisher syndrome (MFS), diabetic neuropathy and with control blood donors. Anti-PMP22 positive sera were detected in 70% of patients with CMT1 and unexpectedly in 60% of patients with CMT2. Interestingly, 44% of the patients with other peripheral neuropathies and 23% of the apparently healthy controls showed also anti-PMP22 antibody reactivity. Immunohistochemical analysis of the human anti-PMP22 antisera on healthy sural nerve sections and on PMP22-expressing COS cells revealed that these sera did not recognise endogenous PMP22. Our results indicate that anti-PMP22 autoantibodies are found in sera of patients with different types of peripheral neuropathies, but their role in the pathogenesis of these diseases remains to be determined.

Adult↗
PubMed2001

Postural sway and diabetic peripheral neuropathy.

The focus of this paper is to evaluate the relationship between postural sway assessed by a gravicorder and peripheral neuropathy in patients with type 2 diabetes. Posturography (GRAVICHART), electrophysiological tests, and power spectrum analysis of heart rate fluctuations were performed in the following age-matched subjects: 123 type 2 diabetic patients without peripheral neuropathy, 32 type 2 diabetic patients with peripheral neuropathy, and 55 healthy control subjects. All diabetic patients with a history of clinical neurological dysfunction were excluded from the study. Significant correlations were found between parameters of GRAVICHART and some parameters of the electrophysiological tests as well as the parameters of heart rate variability. The envelope area and the length per time were larger in type 2 diabetic patients with peripheral neuropathy than in patients without peripheral neuropathy and the control subjects. There were no significant differences in the GRAVICHART parameters between diabetic patients without neuropathy and the healthy control subjects. Type 2 diabetic patients with peripheral neuropathy exhibited an inability to maintain an upright posture. The GRAVICHART can indicate the early stage of postural balance impairment.

Albuminuria↗
PubMed2002

Insensate versus painful diabetic neuropathy: the effects of height, gender, ethnicity and glycaemic control.

AIMS/HYPOTHESIS: To study similarities and differences between people with insensate or painful diabetic peripheral neuropathy, particularly in relation to height, gender, ethnicity and glycaemic control. METHODS: We studied prospectively 2610 patients with Type 2 diabetes attending our Diabetes Centre. Subjects were compared according to degree of sensory loss, and presence or absence of neuropathic pain. The effects of gender and ethnicity were evaluated by studying patients in different height bands. RESULTS: Insensate neuropathy and painful neuropathy was present in 11.4 and 3.3% of subjects, respectively. Age, duration of diabetes, height, vibration perception and HbA(1c) (P<0.0001) were independent determinants of insensate neuropathy, whereas only duration of diabetes and vibration perception (P<0.0001) were predictive of pain. There was more insensate neuropathy in males (OR 1.9) and anglo-celtics (OR 1.4) but stratification by height showed that these effects were due to height. Height has no influence on the development of pain. CONCLUSIONS: There is significant overlap but also considerable dichotomy in the two major forms of diabetic sensory peripheral neuropathy. The insensate type is more explainable by duration, degree of hyperglycaemia and length of peripheral nerves, factors that are likely to reflect severity of underlying structural nerve damage. Glycaemic control was not a predictor of painful neuropathy.

Australia↗
PubMed1986

Autonomic neuropathy: its diagnosis and prognosis.

Autonomic neuropathy is now well established as a relatively common and significant complication of diabetes mellitus. Its importance has been clarified in recent years during which the extent of autonomic control over all areas of body function has been defined. Using simple cardiovascular reflex tests, autonomic abnormalities can be demonstrated without any corresponding symptoms. The often stated concept of 'patchy' involvement in diabetic autonomic neuropathy should now be rejected as too should the view that autonomic neuropathy is either 'present' or 'absent' based on a single test result. When generalized and predominantly metabolic disturbances, as in diabetes, give rise to impaired nerve function, autonomic as well as somatic components of the nerve are affected. Where damage is severe this leads to the characteristic florid picture of symptomatic autonomic neuropathy with its particularly poor prognosis. For the physician in a busy clinic, much of the theoretical and experimental basis for autonomic neuropathy may not appear of direct relevance. However, he has now to be aware of the clinical implications of autonomic damage in the diabetic. This may have particular relevance in the care of the diabetic foot (see Chapter 10), the recognition of many of the vague symptoms associated with autonomic damage, the treatment of disabling features such as postural dizziness and nocturnal diarrhoea, and an awareness of the poor prognosis associated with symptomatic autonomic neuropathy. He will also need to be alert to the dangers of general anaesthesia in such patients, and the possibility of sudden unexpected deaths. Diabetic autonomic neuropathy causes widespread abnormalities, some of which are clinically apparent, some of which can be detected by sensitive tests, and others which have yet to be discovered. Inclusion of the neuropeptides and other hormones within the compass of autonomic control has opened up a whole new area of investigative interest, with many complex interrelationships which still need to be unravelled. This should lead to better understanding of the pathophysiological processes that cause damage to diabetic nerves. With so much research effort directed towards better glycaemic control and aldose reductase inhibitors (see Chapter 8), it may eventually be possible to reverse or prevent this potentially disabling and lethal complication of diabetes.

Autonomic Nervous System Diseases↗
PubMed1996

Management of diabetic pregnancy complicated by coronary artery disease and neuropathy.

Various manifestations of diabetic neuropathy may complicate pregnancies of young diabetic patients. Of all forms of diabetic neuropathy, autonomic neuropathy, and, in particular, gastropathy, may cause the most devastating complications. Because neuropathy is a common abnormality in young asymptomatic diabetic women, screening for this disorder may be advisable and can be accomplished by relatively simple and noninvasive tests. Screening is best performed before conception or early in pregnancy, because pregnancy itself and its possible complications later modify the autonomic nervous function tests and make testing unreliable. Practitioners and obstetricians who provide care and counseling to young diabetic patients should be familiar with the risks and consequences to maternal and fetal health that may be imposed by the different forms of neuropathy. Moderate-to-severe autonomic dysfunction may be considered a relative contraindication to pregnancy, especially if gastropathy is part of the clinical presentation. The management dilemmas and high mortality and morbidity associated with symptomatic diabetic neuropathy may justify the addition of a new independent class, class N (neuropathy), to the current classification systems for diabetes in pregnancy.

Autonomic Nervous System Diseases↗