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Diabetic neuropathies.

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely caused by confusion in the definition and measurement of this disorder. We have reviewed various clinical manifestations associated with somatic and autonomic neuropathy, and we herein discuss current views related to the management of the various abnormalities. Although unproven, the best evidence suggests that near-normal control of blood glucose in the early years after diabetes onset may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose also may lead to reversibility of early diabetic neuropathy, but again, this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, refinements must be made in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.

Diabetes Mellitus↗

Increased prevalence of impaired glucose tolerance in patients with painful sensory neuropathy.

OBJECTIVE: To characterize a cohort of patients with neuropathy and impaired glucose tolerance (IGT) but no other identifiable cause of neuropathy. Of patients with diabetes, 10% have peripheral neuropathy at the time of their diagnosis, suggesting that axonal injury may occur early in the course of glucose intolerance. The American Diabetes Association (ADA) revised diagnostic criteria to recognize IGT (a serum glucose between 140 and 200 mg/dl in a 2-h oral glucose tolerance test [OGTT]) as a risk factor for cardiovascular disease independent of development of diabetes. RESEARCH DESIGN AND METHODS: Using revised ADA criteria for diabetes and IGT, we prospectively evaluated 107 sequential patients with idiopathic neuropathy. RESULTS: A total of 13 of the 107 patients had diabetes, whereas 36 (34%) had IGT, nearly three times the prevalence in age-matched control subjects (P < 0.01). OGTT was often elevated, whereas both fasting plasma glucose and HbA(1c) were normal. Comparing patients with diabetes, IGT, or normal OGTT, age and BMI were similar. However, painful sensory symptoms were more common in patients with IGT and diabetes, and family history of neuropathy was significantly more common in normoglycemic patients. Electrodiagnostic findings of axonal injury were less severe in patients with IGT and were more likely to be confined to sensory fibers than in patients with diabetes. CONCLUSIONS: Our results suggest that IGT may cause or contribute to small-fiber neuropathy, which is similar in phenotype to the painful sensory neuropathy commonly encountered in diabetes. Two-hour OGTT is more sensitive than other measures of glucose handling in screening these patients.

Adult↗

Atrophy of foot muscles: a measure of diabetic neuropathy.

OBJECTIVE: Diabetic neuropathy is a length-dependent process that leads to reduced muscle strength and atrophy of leg muscles in some patients. We hypothesized that intrinsic foot muscles are atrophied in diabetic neuropathy and that the degree of atrophy is a measure of motor dysfunction closely related to the neuropathic process. RESEARCH DESIGN AND METHODS: Consecutive cross-sectional magnetic resonance images of the nondominant foot were obtained for stereological determination of the total volume of the intrinsic foot muscles (VFM) in 23 long-term diabetic patients with (n = 15) and without (n = 8) chronic neuropathy and in 23 matched healthy nondiabetic control subjects. Based on clinical examination, nerve conduction studies, and quantitative sensory examination, a neuropathy rank-sum score was calculated for each patient. RESULTS: Total VFM was 86 +/- 52, 165 +/- 34, and 168 +/- 42 cm3 in neuropathic patients, nonneuropathic patients, and healthy control subjects, respectively (P < 0.001). There was a close inverse relationship between the neuropathy rank-sum score and the VFM (r = -0.75, P < 1 x 10(-5)). CONCLUSIONS: Total volume of the foot muscles is halved in patients with diabetic neuropathy. Atrophy of foot muscles is closely related to the severity of neuropathy and reflects motor dysfunction.

Adult↗

Comparative studies of the induction of erectile response to film and fantasy in diabetic men with and without neuropathy.

The present study deals with the diabetic neuropathies prevailing in men. In this investigation 100 insulin-dependent diabetes mellitus (IDDM) and 314 non-insulin-dependent diabetes mellitus (NIDDM) patients with and without an objective evidence of neuropathy, having an age span in between 15 and 60 years and a duration of diabetes distributed over 1-33 years, were included along with their age-matched nondiabetic controls. The diabetic subjects were evaluated for the induction of erectile responses. Investigation of induction of erectile responses to erotic stimulation by film and fantasy revealed striking results in diabetic patients with established neuropathy. Both IDDM and NIDDM patients with neuropathy exhibited a highly significant decrease (P < .0005) in penile diameter and length, penile arterial pulse amplitude, both systolic and diastolic blood pressures, and heart rate compared to controls of the same age group. However, both IDDM and NIDDM patients without neuropathy showed a nonsignificant difference in the above-mentioned parameters compared to control subjects. A nonsignificant association of induction of erectile responses to erotic stimulations among IDDM and NIDDM patients with and without neuropathy was also observed, suggesting that impotence and altered erectile responses are likely to be associated with an increased frequency to autonomic neuropathy in these patients irrespective of their type of diabetes.

Adolescent↗

An unusual neuropathy in a diabetic patient: evidence for intravenous immunoglobin-induced effective therapy.

We report the case of a 68-year old type-2 diabetic male patient who was admitted to hospital for progressive weakness in the right lower limb. Although his metabolic control was good, he lost more than 20 kg of weight. Despite intensive physio- and vitaminotherapy, his neurological condition kept on degrading with a severe amyotrophy and pain of the right thigh. He was unable to walk and to stand alone. Besides a yet known sensitive polyneuropathy, the electrophysiological study revealed an obvious motor involvement with signs of demyelination and axonal degeneration. Combined with the albuminocytologic dissociation observed in the cerebrospinal fluid, these specific clinical and electrophysiological features led us to postulate a diagnosis of inflammatory neuropathy. The patient underwent a treatment by methylprednisolone and immunoglobins that rapidly induced a striking improvement of his neurological condition. This case report illustrates that rare forms of neuropathy such as inflammatory neuropathies close to chronic inflammatory demyelinating polyneuropathy (CIDP) can occur in diabetic patients and superimpose on the more commonly described forms of neuropathies. It recalls the importance of recognizing CIDP-like neuropathies because unlike other forms of neuropathy, inflammatory neuropathies are perfectly curable.

Aged↗

The change of insulin-like growth factor-1 in diabetic patients with neuropathy.

OBJECTIVE: To evaluate the possible relationship between insulin-like growth factor-1 (IGF-1) and diabetic neuropathy (DNP). METHODS: Sixty-nine patients with Type 2 non-insulin-dependent diabetes (54 with peripheral neuropathy and 15 without neuropathy) were observed. Normal controls were 34 non-diabetic persons. Diabetic peripheral neuropathy diagnosis was carried out taking into account results of NS, ND, NC and AF. After an overnight fast, blood was taken for IGF-1, glucose, hemoglobin Alc, C-peptide, and insulin. Plasma IGF-1 was measured by radioimmunoassay (RIA) method. RESULTS: The neuropathic group had significantly lower levels for IGF-1 (86.43 ng/ml +/- 45.18 ng/ml) compared to normal controls (119.68 ng/ml +/- 89.42 ng/ml) (P < 0.05), and to diabetic patients without neuropathy (113.75 ng/ml +/- 66.58 ng/ml) (P < 0.05). No significant difference was found between diabetic non-neuropathic group and normal control subjects (P < 0.05). In diabetic subjects there was a positive correlation (gamma = 0.27, P < 0.05) between IGF-1 and beat to variation in heart rate. There were negative correlation between IGF-1 and postprandial blood glucose (gamma = -0.3, P < 0.05), and aspartic acid translocase (gamma = -0.27, P < 0.05). CONCLUSION: In diabetic patients with peripheral neuropathy there are abnormalities of IGF-1 that may contribute to the pathogeneses of diabetic neuropathy.

Aged↗

Prevalence of neuropathy in type 2 diabetic patients attending a diabetes centre in South India.

OBJECTIVE: The aim of this study was to determine the prevalence and risk factors for neuropathy among South Indian type 2 diabetic patients attending a diabetes centre. METHODS: One thousand consecutive type 2 diabetic patients attending a diabetes centre in South India were recruited for the study. Biothesiometry studies were performed by a single observer using a biothesiometer. Neuropathy was diagnosed if the vibratory threshold of the great toe exceeded twenty five. RESULTS: Overall, 19.1% of the patients had evidence of neuropathy. The prevalence of neuropathy increased with increase in age (p < 0.001) and duration of diabetes (p < 0.001). Multiple logistic regression analysis revealed age (OR--3.2, 95% confidence interval--2.7-4.1, p < 0.001) and duration of diabetes (OR--1.4, 95% confidence interval--1.2-64, p = 0.001) as the risk factors for neuropathy. CONCLUSION: The overall prevalence of neuropathy in this South Indian type 2 diabetic subjects is 19.1% and age and duration of diabetes are the risk factors for neuropathy.

Adult↗

[Serum alpha-1 antitrypsin levels in patients with Cuban epidemic neuropathy].

INTRODUCTION: Cuban epidemic neuropathy is an emergent disease that due to its magnitude and health problem it was considered the most devastating outbreak of the XX century of the world. On the other hand it has been reported that the protease inhibitor, in particular alpha 1 antitrypsin has importance for the brain metabolic process and its genetic deficiency was produced peripheric neuropathy. Because of it we should decided to study the serum levels of patients suffering from this disease. PATIENTS AND METHODS: It has been studied serum alpha 1 antitripsin levels in 39 patients with peripheric Cuban epidemic neuropathy, six patients with the mixt variant of the disease and 10 patients with diabetic neuropathy. All patients has no toxic habits like alcohol and tobacco consumption. The quantification of alpha 1 antitrypsin was performed by radial immunodiffusion. RESULTS: When the median values of alpha 1 antitrypsin were compared no significant differences were obtained among the different neuropathies with a significance levels less than 0.05. There was a significant increased of apha 1 antitrypsin with the evolution time of the disease in the patients with the mixt variant and a significant correlation between alpha 1 antitrypsin levels and age with diabetic neuropathy. CONCLUSIONS: This protease inhibitor looks to be involved in the physiopathology of the Cuban epidemic neuropathy with a decreased levels during the initial time of the disease.

Age Factors↗

[Diagnosis of hereditary neuropathies in adult-subjects].

The clinical approach to hereditary neuropathies of adulthood has become very complex. The following issues are reviewed: 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. It is useful to identify different phenotypes 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 (CMT) disease, familial amyloid polyneuropathy (FAP), hereditary sensory and autonomic neuropathy, Fabry disease, Tangier disease, porphyric neuropathies, Refsum disease, hereditary neuropathy with liability to pressure palsies (HNPP), hereditary neuralgic amyotrophy and other rare disorders involving the peripheral nervous system are reviewed.

Adult↗

[Postprandial hypotension and autonomic neuropathy in diabetic patients].

UNLABELLED: Postprandial hypotension is commonly defined as the decrease in systolic blood pressure of 20 mm Hg and more, observed within 2 hours after meal ingestion. This phenomenon was described in subjects with comprised function of autonomic nervous system. However, the data on its prevalence in diabetic patients are scarce. The aim of the study was to assess the concordance of postprandial hypotension and autonomic cardiovascular neuropathy in diabetes mellitus. The study included 67 patients (26 males, 41 females, mean age: 47.5 +/- 16.2 years) with diabetes type 1 or 2 (mean disease duration: 13.3 +/- 8.8 years), treated with diet and insulin injections. Postprandial hypotension was diagnosed based on results of automatic blood pressure recordings performed within 90 minutes after test meal ingestion. Tests of Ewing's battery were used to evaluate autonomic cardiovascular neuropathy. RESULTS: Mean postprandial decrease in systolic blood pressure of 17.7 +/- 11.7 mm Hg was noted at 48.0 +/- 13.7 min after meal ingestion. The study patients were divided into 2 groups based on results of systolic blood pressure recordings. In group A of 39 subjects (58.2%) the mean fall in systolic blood pressure of 8.9 +/- 4.4 mm Hg was observed. In group B of 28 (41.8%) subjects fulfilling the criteria of postprandial hypotension systolic blood pressure decreased after the meal of 30.0 +/- 6.2 mm Hg, the difference between groups was statistically significant (p < 0.001). Autonomic cardiovascular neuropathy was recognized in 41 (61.2%) of the study patients. The more advanced neuropathy was stated in group B (neuropathy scale score: group A--1.54 +/- 1.48 points, group B--5.11 +/- 1.93 points, p < 0.001). Statistically significant correlation between the magnitude of postprandial systolic blood pressure fall and cardiovascular neuropathy scale score was noted (Spearman's correlation co-efficient R: -0.612: p < 0.01). Postprandial blood pressure fall correlated significantly with orthostatic systolic blood pressure changes (correlation co-efficient R: 0.610; p < 0.001). CONCLUSIONS: Postprandial hypotension is an important symptom of diabetic cardiovascular neuropathy. It is recommended to include postprandial blood pressure measurements in diagnostic algorithm of autonomic nervous system dysfunction in diabetic patients.

Adult↗

Diabetic neuropathy--choices of treatment.

Diabetic neuropathy represents a heterogeneous pathology taking place during diabetes mellitus (DM) evolution, hiding possibilities for rapid evolution which threaten even the life of the diabetic person. As a result, the recognition as precocious as possible of the neuropathy-induced alterations and the ways of treating this complication are essential. Diabetic neuropathy is classified in peripheral and vegetative, each of them with numerous clinical forms. Nevertheless, its etiopathogeny remains not totally understood, many theories existing for explaining it, its development being probably the result of a mixture of pathogenic mechanisms. Although there are difficulties in appreciation of the neuropathy prevalence in diabetic people, it is generally known that this alteration is one of the most frequent and invalidant major complication that affects this population, treatment as precocious as possible being essential. alpha-lipoic acid, substance with antioxidant properties, plays a central role in the energetic metabolism, principally functioning as a coenzyme in multienzymatic mitochondrial complexes alpha-lipoic acid has complex actions on different levels of the human organism, having many indications in different diseases, including DM. The results of numerous clinical studies have confirmed its efficacy in treating diabetic neuropathy. The present study has proposed itself to investigate the long-term effect of the short-term i.v. treatment with Thiogamma 600 (alpha-lipoic acid) in patients having type I or 2 DM, proving neuropathy symptoms and signs reduction evaluated in 3 months time, without metabolic control of the disease. If this amelioration proves to be persistent in time, with or without continuing the medication, this treatment will represent the most evident and efficient present solution in neuropathy.

Adult↗

Effects of 3-month treatment with the antioxidant alpha-lipoic acid in diabetic peripheral neuropathy.

Alpha lipoic acid is a natural antioxidant that has been suggested to improve symptoms of diabetic neuropathy. To assess these potential benefits, a cohort of 26 type 2 diabetic patients with symptomatic peripheral neuropathy (stage 2) received a daily dose of 600 mg alpha-lipoic acid, and were followed for a 3 month-period. No dropout was noted. At the end of the follow-up period, in 20 subjects (76.9%) there was a 1-stage regression of somatic neuropathy (from symptomatic to asymptomatic neuropathy, and in 5 patients (19.2%) no signs of neuropathy were found. The nerve conduction velocity of motor fibers improved from 36.8 (95% Confidence Interval CI = 30.9-42.7) meters/second to 41.3 (95% CI = 39.5-43.0) meters/second (p = 0.049, paired t test). Mean blood glucose measured was significantly lower at 3 months than at baseline [197.9 (95% CI = 170.1-225.7) versus 162.2 (95% CI = 146.1-178.2 mg/dl, p = 0.02, paired t test)]. In a multiple linear regression model with age. sex, body mass index, diabetes duration and the difference between blood glucose values at 3 months and at baseline as explanatory variables, the increment in nerve conduction velocity was not accounted for by the improved glycemic control. Women, thinner and younger patients tended to benefit more from the treatment in terms of nervous conduction velocity improvement. In conclusion, alpha-lipoic acid seems to be efficient and safe in the treatment of diabetic peripheral neuropathy, improving both clinical manifestations and nerve conduction velocity. Placebo controlled clinical trials are needed to further define the role of this new medication in the treatment of diabetic neuropathies.

Antioxidants↗

Advances in diabetes for the millennium: new treatments for diabetic neuropathies.

Diabetic neuropathies are not a single disorder but a heterogeneous group of conditions that involves different parts of the somatic and autonomic nervous systems. Neuropathies may be focal or diffuse, proximal or distal. The focal neuropathies are either entrapment syndromes that occur in 30% of patients with diabetes, and if recognized can be treated with diuretics, splinting local steroids, and unentrapment. The focal mononeuritides are vascular assaults and heal spontaneously and need supportive therapy. The proximal neuropathies are, for the most part, inflammatory demyelinating conditions that occur 11 times more frequently in the diabetic population and respond well to intravenous immunoglobulin (Ig)G or immunosuppressive treatments. The distal symmetric polyneuropathies are usually a mixed picture of sensorimotor dysfunction, and recent evidence based on intraepidermal nerve-fiber changes has identified a subset of painful neuropathies that are associated with impaired glucose tolerance and dysmetabolic syndrome, and precede the onset of diabetes. Pain in neuropathy is also multifactorial and can occur at different levels, starting at the peripheral sympathetic nervous system in the skin (C fibers) and migrating to involve A-beta and A-delta fibers to produce allodynia, continuing with reorganization at the cord-level, cold allodynia, and finally, within the central nervous system, spontaneously as opposed to provoked pain. This is best treated with agents that target the different levels of pain production. It now seems that the pathogenesis of diabetic neuropathy is also heterogeneous with causative factors, including microvascular insufficiency, oxidative stress, nitrosative stress, defective neurotrophism, and autoimmune-mediated nerve destruction. New therapies are aimed at the underlying pathogenesis as well as the symptom complex. If attention is directed toward a pathogenetic approach, much can be done to alleviate the symptoms, alleviate the mitigation of quality of life, and now it would seem to address the underlying biological disturbance.

Diabetic Neuropathies↗

[Prospective study of cardiac autonomic neuropathy in diabetes mellitus].

For assessment of clinical and prognostic values of cardiac autonomic neuropathy, 53 patients with diabetes mellitus were followed-up for five years. Parasympathetic innervation was assessed by recording heart rate variability during deep breathing, Valsalva manoeuvre and lying-to-standing while sympathetic function was evaluated by measuring postural change in systolic blood pressure. During the follow-up period 1 of 23 diabetic patients died in group without signs of cardiac autonomic neuropathy whereas 2 of 13 diabetics and 10 of 17 diabetics deceased in groups with mild and definitive signs of cardiac autonomic neuropathy, respectively. At reinvestigation, the values of tests for parasympathetic impairment worsened or did not change significantly while improvement in these tests was only exceptionally observed in 40 diabetic patients. No significant change in values of test for sympathetic function was documented during the follow-up period suggesting that parasympathetic (vagal) impairment might precede the sympathetic dysfunction during development of autonomic neuropathy in diabetic patients. No correlation was observed between changes in cardiac autonomic neuropathy and alterations in distal somatic neuropathy (assessed by measurement of motor nerve conduction velocity in peroneal nerves) during the prospective study. Definitive cardiac autonomic neuropathy--as one of the late complications of diabetes mellitus--suggests poor prognosis in diabetic patients.

Adult↗

Impact of microangiopathy on chronic symptomatic peripheral neuropathy.

The role of microvascular disease in the aetiology of diabetic peripheral neuropathy remains controversial. Muscle capillary basement membrane thickening (MCBMT) and increased albumin excretion rates (AER) are features of generalized diabetic microangiopathy and may relate to the severity of neuropathy. We have studied 19 patients with neuropathy of greater than 12 months duration and assessed relationships between the severity of neuropathy and MCBMT, AER, presence of retinopathy, age and duration of diabetes. Nine patients had retinopathy and 10 did not. The two groups of patients were well matched for age, type of diabetes and HbA1% but diabetic patients with retinopathy had significantly longer duration of diabetes (median duration 22 yr, range 3-42 yr compared with patients without retinopathy (6 yr range 1-20 yr p less than 0.05). The group with retinopathy had significantly greater median MCBMT 3,077 A (range 741-10,732 A) than their age matched non-diabetic controls 2,256 A (1,290-4,406 A p less than 0.02) or the 10 diabetic patients without retinopathy 1,599 A (805-5,152 A). The patients with retinopathy also had greater median AER 88 micrograms/min (range 8-200 micrograms/min) compared with patients without retinopathy 8 micrograms/min (2-63 micrograms/min p less than 0.05), and had significantly more severe neuropathic features on a 12 point neurophysiological ranking scale (p less than 0.05). This study showed an association between retinopathy and severity of neuropathy but there were no associations between severity of neuropathy or AER with MCBMT. Severe chronic peripheral neuropathy is associated with microangiopathic complications.

Albuminuria↗

Pathogenesis of diabetic neuropathy: role of altered phosphoinositide metabolism.

A unifying metabolic hypothesis completely accounting for the development of one or more of the chronic complications of diabetes on the basis of a single aspect of disturbed glucose metabolism resulting from insulin deficiency and/or hyperglycemia has been sought by clinical and basic scientists for decades. A growing body of loosely related but internally consistent scientific data obtained from cultured cells, incubated tissue preparations, animal models, and man implicate sorbitol- and glucose-induced myo-inositol depletion and altered phosphoinositide metabolism in a series of secondary biochemical, functional, and architectural abnormalities in the PNS in diabetes. These early metabolically based functional and structural changes simulate those that characterize human diabetic neuropathy. Can abnormal phosphoinositide metabolism in diabetic nerve thereby by itself explain the development of chronic diabetic neuropathy with all of its clinical complexity and heterogeneity? Almost certainly not. Even if the entire contribution of hyperglycemia to the development of diabetic neuropathy were mediated by secondary abnormalities in phosphoinositide metabolism, other factors must also play a role. Witness the differences in the histopathological picture of neuropathy in patients with IDDM and NIDDM despite similar durations and severity of diabetes, the apparent influence of age and gender on the appearance of early neuropathy in patients with IDDM, and the association of alcohol consumption with diabetic neuropathy. While early metabolic and functional disturbances in diabetic nerve such as impaired (Na,K)-ATPase function and paranodal swelling are empirically attributable to abnormal myo-inositol and phosphoinositide metabolism, more advanced abnormalities such as axo-glial dysjunction may reflect superimposed independent biochemical and/or hormonal defects (although, as mentioned previously, aldose reductase inhibition decreases axo-glial dysjunction in diabetic humans). The PNS has only a limited repertoire of responses to a variety of insults, so that Wallerian degeneration, axonal atrophy, impaired axonal transport, and dystrophic changes in diabetic neuropathy may represent multiple factors. On the other hand, the increasingly recognized importance of the phosphoinositide cascade in neuromodulation may attribute a progressively wider range of disturbances in the diabetic PNS to myo-inositol depletion and associated defects in phosphoinositide metabolism. Thus, while all effects of aldose reductase inhibitors in the PNS of diabetic rats have been reproduced by myo-inositol supplementation when this alternative intervention has been tested, the exact role of phosphoinositide metabolism in most of these responses is not well understood.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

[Tomaculous neuropathy. A histopathological study and electroclinical correlates in 10 cases].

Among 980 sural nerve biopsies, the nerves of 10 patients showed a great number of focal sausage-shaped thickenings of the myelin sheaths and were investigated by light and electron microscopy, teasing and quantitative studies. Single teased nerve fibres revealed myelin thickening in more than 25 p. 100 of internodes. This condition defined the tomaculous neuropathy and differed from other degenerative or toxic neuropathies which displayed a small number of internodes with myelin thickenings, in less than 5 p. 100. Segmental demyelination and remyelination were found in 12 p. 100 to 65 p. 100 of myelinated fibres. Tomaculous swellings were observed in the internodes of these fibres. Except axonal constriction within the sausage-shaped thickenings, no fibers with axonal degeneration was observed. The density of myelinated and unmyelinated fibres was normal. The loss of large myelinated fibres was interpreted as resulting from the myelinic changes. Clinical and electrophysiological data were similar in the ten cases of tomaculous neuropathies and in hereditary neuropathy with liability to pressure palsies, i.e.: autosomal dominant inheritance, higher incidence in males, recurrent nerve trunck and/or brachial plexus involvement related to compression, slowing of nerve conduction velocities in clinically affected and unaffected nerves more pronounced in anatomical narrow sites and increased F wave latencies. One patient (case 10) showed a mixed sensory motor progressive neuropathy but signs of widespread neuropathy were noted in more advanced cases. A great number of tomaculous swellings of myelin sheaths is considered as a specific but non constant change of hereditary neuropathy with liability to pressure palsies.

Electrophysiology↗

Study of the cutaneous electric potentials and the perception threshold to an electric stimulus in diabetic patients with and without clinical neuropathy.

Clinical heterogeneity of diabetic peripheral neuropathy could express a neurophysiological and electrophysiological heterogeneity possibly related with the dissociated metabolic susceptibility of the difference types of nerve fibres and endings. To evaluate the functional status of the skin autonomous nervous system and of the deep pain sensitivity system in diabetics we studied two electrophysiological parameters skin electrical potential (using Digital Multimeter 3466 Hewlet Packard, USA) and the perception threshold (microA) at an electrical stimulus (spike wave, 0.5 m sec duration) 1 cm deeply applied through 2 acupuncture needles placed 30 cm distance each other, in 3 groups: Ia-18 diabetic patients with clinical signs of neuropathy (12 M, 6 F, aged 55 +/- 17 yrs); Ib - 17 diabetic patients without clinical signs of diabetic neuropathy (12 M, 5 F, aged 57 +/- 16 yrs); I1 - 10 age and sex matched non-diabetic controls. Our data show: a higher mean value of the potential in the acupuncture points as against neighbour areas, both in non-diabetic control (- 111 +/- 25 mV v.s. -81 +/- 29 mV, p less than 0.05) and in diabetics (-85 +/- 43 mV v.s. -58 +/- 25 mV, p less than 0.01); a lower mean value of the electrical potentials in diabetic with clinical signs of neuropathy as against in those without clinical signs of neuropathy (-66 +/- 29 mV v.s. -108 +/- 43 mV, p less than 0.01): a higher mean value of the perception threshold in diabetics with clinical signs of neuropathy as against in diabetics without clinical signs of neuropathy (213 +/- 82 microA. v.s. 102 +/- 40 microA, p less than 0.01); a significant correlation (r = -0.81) between the perception threshold and the electrical potentials of the studied points.

Adult↗