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PubMed1984

Blood flow patterns in painful diabetic neuropathy.

Peripheral blood flow is known to be qualitatively increased in diabetic patients with neuropathy. We have measured the actual blood flow in the feet of diabetic patients with neuropathy using non-invasive mercury strain gauge plethysmography and Doppler sonogram techniques and shown that it is increased on average five times above normal at an ambient temperature of 20 degrees-22 degrees C. Moreover, reduction of this high flow by sympathetic arousal stimuli proved possible in those with severe painful neuropathy contrasting strongly with failure to reverse it in those with severe non-painful sensory neuropathy. Reduction of blood flow was associated with reduction in neuropathic pain. We studied 22 diabetic patients with severe sensory neuropathy and eight with painful neuropathy. High resting foot blood flows were demonstrated in both groups with neuropathy. The big toe flow in those with severe sensory neuropathy was 29.3 +/- 9.2 ml X min-1. 100 ml-1 (mean +/- SD) and in the painful neuropathy group, 25.9 +/- 7.5, compared with 5.2 +/- 2.4 ml X min-1 X 100 ml-1 in the non-diabetic control subjects (p less than 0.001). High foot skin temperatures were also recorded in the groups with neuropathy, reflecting the high blood flow. The subjects with painful neuropathy retained the ability to constrict peripheral blood vessels in response to arousal stimuli, and reduce peripheral flow on average by 32% compared with the patients with sensory neuropathy who responded on average by only 10%. The demonstration of a peripheral sympathetic defect, responsible for the high blood flow and the potential reversal of such flow in painful neuropathy may be important in our further understanding of the aetiology of such pain and its treatment.

Adult↗
PubMedDate not supplied

Medial arterial calcification and diabetic neuropathy.

The aim of this study was to detect linear arterial calcification (Mönckeberg's sclerosis) localized in feet, ankles, legs, knees and hands in an attempt to correlate the extent of calcification with the presence and severity of autonomic neuropathy as well as with microangiopathy (proliferative retinopathy, proteinuria greater than 200 mg/die) and peripheral neuropathy. Typical linear calcification were observed in 37 out of 41 (90.2%) patients with autonomic neuropathy and in none of those without autonomic neuropathy (p less than 0.001). These 37 patients were divided into two subgroups by cluster analysis: Subgroup A, including 18 subjects with calcification length ranging from 8 to 26 cm and moderate autonomic neuropathy, and Subgroup B, including 19 subjects with calcification length between 58 and 126 cm and severe autonomic neuropathy (p less than 0.0001 by Spearman's test). No difference in the length of arterial calcification was detected between patients with proteinuria greater than 200 mg/24h and/or proliferative retinopathy and patients without these complications. A possible relationship between arterial calcification and peripheral neuropathy is difficult to evaluate; in fact, the majority of subjects having autonomic neuropathy had peripheral neuropathy, too. Vice versa, around 10% of patients without peripheral neuropathy but with autonomic neuropathy did not have Mönckeberg's sclerosis. Autonomic neuropathy is the principal factor responsible for calcification of the arterial media, and in addition the severity of the neuropathy, rather than the patient's age or the known disease duration seems to determine the extent of calcification.

Adult↗
PubMed1995

The prevalence of autonomic and peripheral neuropathy in insulin-treated diabetic subjects.

The prevalence of autonomic and peripheral neuropathy was examined in 506 diabetic subjects treated with insulin, mean age 43 years, diabetes duration 15 (range 1-54) years. Autonomic neuropathy was present if two or more (of four) cardiovascular autonomic function tests were abnormal using age-related ranges derived from 310 normal control subjects. Peripheral neuropathy was defined as a vibration threshold > 95th centile for age combined with absent/impaired ankle reflexes. Eighty-four (16.6%) of diabetic subjects had abnormal autonomic function and 119 (23.5%) peripheral neuropathy, concordant in 44/506 (8.7%). Of the diabetic subjects with autonomic neuropathy 40/84 (47.6%) did not have peripheral neuropathy and only 44/119 (37.0%) with peripheral neuropathy had abnormal autonomic function (p < 0.001). The prevalence of both neuropathies increased in relation to diabetes duration (both p < 0.001). Autonomic neuropathy was more common in subjects diagnosed < 20 years of age (18.2%) vs age > 40 years (11.1%) (p < 0.05). In contrast peripheral neuropathy was more common with older age at diagnosis (< 20 years 13.5% vs 36.8% > 40 years, p < 0.001). The age-related prevalence of autonomic neuropathy peaked at age 40-49 years while peripheral neuropathy increased progressively with age (p < 0.001). The prevalence of peripheral exceeded autonomic neuropathy 20 years after diagnosis (40.2% vs 30.7%, p < 0.001).

Adult↗
PubMed2002

[Predictors for diabetic neuropathy according to applied criteria of its diagnosis].

It is difficult to establish predictors for diabetic neuropathy because no generally accepted criteria of its diagnosis exist. In previous investigations risk factors profiles for neuropathy differ markedly. The aim of this study was to assess risk predictors for diabetic neuropathy in relation to different criteria of its diagnosis. Ninety-five diabetic patients entered the study. The exclusion criteria included uremia, alcohol abuse and radiculopathy. Control group consisted of 43 healthy volunteers. All patients underwent the clinical assessment, instrumental evaluation of superficial and deep sensation, tests of cardiovascular autonomic function and nerve conduction studies. According to the performed assessment patients were classified into following groups: without neuropathy, suspicion of neuropathy, neuropathy confirmed in clinical examination, neuropathy confirmed in electrophysiological testing, autonomic neuropathy. Analysis showed that the most important predictors in patients with subjective symptoms were type 2 diabetes mellitus, diabetes duration and age of patients. When neuropathy was diagnosed according to the clinical examination, predictors included type 2 diabetesmellitus and duration of the disease. In the cases of neuropathy confirmed by electrophysiological studies and autonomic neuropathy, only diabetes duration appeared to be a significant predictor. Our study demonstrated that predictors for diabetic neuropathy varied in relation to different diagnostic criteria and where the most important predictor for all forms of neuropathy is duration of diabetes. This result indicates the need for frequent screening tests in patients with long duration of the disease, irrespective of its metabolic control, patients' age or type of diabetes.

Adolescent↗
PubMed1995

Triphenylphosphite neuropathy in hens.

Single doses of triphenyl phosphite (TPP), a triester of trivalent phosphorus, cause ataxia and paralysis in hens. Characteristics of neurotoxicity were described as somewhat different from organophosphate induced delayed polyneuropathy (OPIDP), which is caused by triesters of pentavalent phosphorus. The onset of TPP neuropathy was reported to occur earlier than that of OPIDP (5-10 versus 7-14 days after dosing, respectively), and chromatolysis, neuronal necrosis and lesions in certain areas of the brain were found in TPP neuropathy only. Pretreatment with phenylmethanesulfonyl fluoride (PMSF) protects from OPIDP, but it either partially protected from effects of low doses or exacerbated those of higher doses of TPP. In order to account for these differences with OPIDP, it was suggested that TPP neuropathy results from the combination of two independent mechanisms of toxicity: typical OPIDP due to inhibition of neuropathy target esterase (NTE) plus a second neurotoxicity related with other target(s). We explored TPP neuropathy in the hen with attention to the phenomena of promotion and protection which are both caused by PMSF when given in combination with typical neuropathic OPs. When PMSF is given before neuropathic OPs it protects from OPIDP; when given afterwards it exaggerates OPIDP. The former effect is due to interactions with NTE, the latter to interactions with an unknown site. The time course of NTE reappearance after TPP (60 or 90 mg/kg i.v.) inhibition showed a longer half-life when compared to that after PMSF (30 mg/kg s.c.) (10-15 versus 4-6 days, respectively). The clinical signs of TPP neuropathy (60 or 90 mg/kg i.v.) were similar to those observed in OPIDP, appeared 7-12 days after treatment, correlated with more than 70% NTE inhibition/aging and were preceded by a reduction of retrograde axonal transport in sciatic nerve of hens. TPP (60 mg/kg i.v.) neuropathy was promoted by PMSF (120 mg/kg s.c.) given up to 12 days afterwards and was partially protected by PMSF (10-120 mg/kg s.c.) when given 24 h before TPP (60 or 90 mg/kg i.v.). The previously reported early onset of TPP neuropathy might be related to the higher dose used in those experiments and to the resulting more severe neuropathy. The lack of full protection might be explained by the slow kinetics of TPP, which would cause substantial NTE inhibition when PMSF effects on NTE had subsided. Since PMSF also affects the promotion site when given before initiation of neuropathy, the resulting neuropathy would then be due to both protection from and promotion of TPP effects by PMSF. No promotion by PMSF (120 mg/kg s.c.) was observed in TPP neuropathy (90 mg/kg i.v.) partially protected by PMSF (10-30 mg/kg s.c.). This might also be explained by the concurrent effects on NTE and on the promotion site obtained with PMSF pretreatment. We conclude that TPP neuropathy in the hen is likely to be the same as typical OPIDP. The unusual effects of combined treatment to hens with TPP and PMSF are explained by the prolonged pharmacokinetics of TPP and by the dual effect of PMSF i.e. protection from and promotion of OPIDP.

Animals↗
PubMed2004

[Paraneoplastic peripheral neuropathies].

Paraneoplastic peripheral neuropathies constitute a heterogeneous group of conditions. A link between the tumor and the neuropathy has been demonstrated in a subgroup only. Definite paraneoplastic neuropathies correspond to neuropathies associated with antibodies reacting with antigens common to the peripheral nervous system and the cancer. Neuropathies associated with anti-Hu antibodies are the most frequent and consist mainly in subacute sensory neuronopathy. Sensory or sensory-motor neuropathies with anti-CV2 antibodies are less frequent. The link between the cancer and the neuropathy is less clear in the other forms. The frequency of cancer in this group varies from 1 to 18 p.cent.These neuropathies include inflammatory demyelinating neuropathies, neuropathy and vasculitis, lower motor neurone diseases, and autonomic neuropathies. Occasionally, the neuropathy improves with treatment of the tumor. Recent data suggest that gangliosides may be the target of the immune process in neuropathies associated with melanoma.

Autoantibodies↗
PubMed2006

Neuropathy associated with gluten sensitivity.

OBJECTIVES: To prospectively study the clinical, neurophysiological and neuropathological characteristics of axonal neuropathies associated with positive antigliadin antibodies and the prevalence of such neuropathies in a cohort of patients with sporadic axonal neuropathy. METHODS: Prospective screening (using antigliadin, antiendomysium and tissue transglutaminase antibodies) of patients with peripheral neuropathy attending a neurology clinic. RESULTS: 215 patients with axonal neuropathy were screened. 141 patients had symmetrical sensorimotor neuropathy, 47 had mononeuropathy multiplex, 17 had motor neuropathy and 10 had small-fibre neuropathy. Despite extensive investigations of the 215 patients, 140 had idiopathic neuropathy. Positive immunoglobulin (Ig)G with or without IgA antigliadin antibodies was found in 34% (47/140) of the patients with idiopathic neuropathy. This compares with 12% prevalence of these antibodies in the healthy controls. The prevalence of coeliac disease as shown by biopsy in the idiopathic group was at least 9% as compared with 1% in the controls. The clinical features of 100 patients (47 from the prevalence study and 53 referred from elsewhere) with gluten neuropathy included a mean age at onset of 55 (range 24-77) years and a mean duration of neuropathy of 9 (range 1-33) years. Gluten-sensitive enteropathy was present in 29% of patients. The human leucocyte antigen types associated with coeliac disease were found in 80% of patients. CONCLUSIONS: Gluten sensitivity may be aetiologically linked to a substantial number of idiopathic axonal neuropathies.

Adolescent↗
PubMed1999

Carcinoma associated paraneoplastic peripheral neuropathies in patients with and without anti-onconeural antibodies.

OBJECTIVE: When to suspect a paraneoplastic disorder is a puzzling problem that has not recently been studied in a large series of patients referred for peripheral neuropathy. METHODS: From 422 consecutive patients with peripheral neuropathy, 26 were analysed who concomitantly had carcinoma but no tumorous infiltration, drug toxicity, or cachexia. Their clinical, pathological, and electrophysiological data were analysed according to the presence of anti-onconeural antibodies, the latency between presentation and cancer diagnosis, and the incidence of carcinoma in the corresponding types of neuropathy of the population of 422 patients. RESULTS: Seven patients (group I) had anti-onconeural antibodies (six anti-Hu, one anti-CV2) and 19 did not (groups IIA and B). In group I, subacute sensory neuropathy (SSN) was the most frequent but other neuropathies including demyelinating neuropathies were present. Patients in group II A had a short latency (mean 7.88 months), and a rapidly and usually severe neuropathy which corresponded in 11/14 to an established inflammatory disorder including neuropathy with encephalomyelitis, mononeuritis multiplex, and acute or chronic inflammatory demyelinating polyneuropathy (CIDP). Patients in group IIB had a long latency (mean 8.4 years) and a very chronic disorder corresponding in four of five to an axonal non-inflammatory polyneuropathy. In this population, the incidence of carcinoma occurring with a short latency was 47% in sensory neuronopathy, 1.7% in Guillain-Barré syndrome, 10% in mononeuritis multiplex and CIDP, and 4.5% in axonal polyneuropathy. CONCLUSIONS: Paraneoplastic neuropathies associated with carcinoma are heterogeneous disorders. Neuropathies occurring with a long latency with tumours probably resulted from a coincidental association. Neuropathies which occurred within a few years of the tumour evolved rapidly and corresponded mostly to inflammatory disorders. As dysimmune neuropathies are probably paraneoplastic in a limited number of cases, patients with these disorders should probably not be investigated systematically for carcinoma in the absence of anti-onconeural antibodies, except when the neuropathy is associated with encephalomyelitis and probably with vasculitis. Questions remain concerning CIDP.

Aged↗
PubMed2006

Peripheral neuropathy induced by microtubule-stabilizing agents.

Microtubule-stabilizing agents (MTSAs), including the taxanes and epothilones, are effective chemotherapeutic agents for the treatment of many cancers. Neuropathy is a major adverse effect of MTSA-based chemotherapy, with severe peripheral neuropathy (grade 3 or 4) occurring in as many as 30% of patients treated with a MTSA. MTSA-induced neuropathy usually resolves gradually after cessation of the treatment. The most reliable method to accurately assess MTSA-induced neuropathy is by clinical evaluation, although additional techniques are being developed and evaluated. Among MTSA-induced neuropathy, the most extensively studied is that induced by taxanes; such a neuropathy usually presents as sensory neuropathy and is more common with paclitaxel than docetaxel. The incidence of MTSA-induced neuropathy seems to depend on the MTSA dose per treatment cycle, the schedule of treatment, and the duration of the infusion. Although there have been several small clinical trials with neuroprotective agents, early recognition and supportive care are the best approaches for prevention and management of MTSA-induced neuropathy. In the future, research should focus on elucidating the mechanism of MTSA-induced neuropathy, developing reliable in vivo and in vitro preclinical models to study MTSA-induced neuropathy, developing a more reliable grading system for MTSA-induced neuropathy, developing more reliable methods for evaluating MTSA-induced neuropathy, and evaluating the efficacy of potential neuroprotective agents in clinical trials.

Albumin-Bound Paclitaxel↗
PubMed2005

[Differential diagnosis of peripheral neuropathy].

Neuropathies can be caused by metabolic-endocrine, toxic, and hereditary disorders, various conditions of nutrition deficiency, inflammatory or systemic diseases, vasculopathies, and they can be part of the paraneoplastic symptomatology as well. Diabetes mellitus (DM) is the most common cause of neuropathy in our population. Diabetic polyneuropathy represents the most frequent form of polyneuropathy in well-developed countries, indicates more admissions that other diabetic complications and has important impact on the quality of patients' life. From the differential diagnostic point of view, it is important that signs of the diabetic neuropathy are non-specific and identical for all neuropathies. Each neuropathy represents complex of sensory, motor and vegetative signs. In addition to the clinical features, biochemical and paraclinical investigations are conclusive for identifying the etiology of neuropathy. Suspicion for non-diabetic etiology of neuropathy is increased in neuropathy developed earlier to DM, neuropathy in very good controlled DM, and asymmetric neuropathy. After elucidation of an atypical neuropathy signs, neurological and electromyographical studies should follow. With the development of serological and genetic tests, autoimmune and hereditary neuropathies are increasingly diagnosed in cases of to that time unclassified idiopathic neuropathies. Even after complex investigation procedures, the etiology of polyneuropathy remains unrevealed in approximately 50% of cases.

Diagnosis, Differential↗
PubMed1990

Morphometry of endoneurial capillaries in diabetic sensory and autonomic neuropathy.

Nerve biopsies were obtained from 27 patients with diabetic neuropathy. All had a symmetric distal sensory and autonomic neuropathy or a purely sensory neuropathy. Mean age was 39.8 years (range 23-57 years). Two patients had Type 2 (non-insulin-dependent) diabetes mellitus and the remainder Type 1 (insulin-dependent) diabetes. Morphometric observations on endoneurial capillaries were compared with results from organ donor control cases and from patients with type 1 hereditary motor and sensory neuropathy. The area of the lumen of the capillaries did not differ between the three groups. The area occupied by the capillary endothelial cells in transverse section and the number of endothelial cell nuclei were increased both in the patients with diabetic neuropathy and hereditary motor and sensory neuropathy, as was the thickness of the surrounding basal laminal zone. 'Closure' of endoneurial capillaries in diabetic neuropathy, reported in another study, was not confirmed. Capillary density and nearest-neighbour distances were similar in the diabetic and organ donor control cases. Capillary density was reduced in the patients with hereditary motor and sensory neuropathy, this being related to increased fascicular area consequent upon the presence of hypertrophic changes. The presence of thickening of the pericapillary basal laminal zone and endothelial cell hyperplasia both in diabetic and hereditary motor and sensory neuropathy, the latter being a neuropathy in which a vascular basis can be discounted, makes it difficult to use such changes as an argument favouring a vascular cause for diabetic neuropathy. There were differences in the basal laminal zone between the diabetic and hereditary motor and sensory neuropathy cases suggesting that the reduplicated basal lamina was more persistent in the diabetic patients.

Adult↗
PubMed2002

Symptomatic diabetic and non-diabetic neuropathies in a series of 100 diabetic patients.

We have reviewed the clinical and pathological data of a series of 100 consecutive diabetic patients with symptomatic neuropathy in order to learn more about the causes of neuropathy in this population and on the signs and symptoms that could suggest another cause than diabetes in this setting. After diagnostic procedures, patients were assigned one (at most two) of a final total of 18 different causes of neuropathy. Diabetes accounted for 74 % of the neuropathies in the whole group of patients and for 79 % of those with a fiber length dependent pattern of neuropathy. One third of patients had a neuropathy unrelated to diabetes. As a group, 71 % of the patients presented either a length dependent diabetic polyneuropathy (LDDP) or a proximal diabetic neuropathy (PDN). The LDDP group was biased towards more severely affected patients owing to our specialization. Conversely, most patients with proximal diabetic neuropathy had usual features. Chronic inflammatory demyelinating neuropathy that was diagnosed in 9 % of the patients was the most common non-diabetic cause of neuropathy in this population. We conclude that a short interval between diagnosis of diabetes and the onset of the neuropathy, early motor deficit, markedly asymmetrical deficit and generalized areflexia, which are all uncommon in the LDDP, argue in favor of a non diabetic origin of the neuropathy and should lead to further investigation.

Adult↗
PubMed1988

HLA-antigens and immunity to insulin in insulin-dependent diabetics with or without diabetic neuropathy.

In order to define genetic, immunological and metabolic risk factors and markers associated with diabetic neuropathy (DN) 47 insulin-dependent diabetic patients with neuropathy were compared to 30 age-matched insulin-dependent diabetes mellitus (IDDM) patients without neuropathy. Patients with diabetic neuropathy more often had proliferative retinopathy and Albustix positive proteinuria than patients without neuropathy. Judged by haemoglobin A1 (HbA1) concentrations measured during the preceding two years glycaemic control was worse in patients with than without diabetic neuropathy. The frequency of HLA-antigens DR3, DR4, DR3/DR4, B8, and B15 were increased and those of DR2 and B7 decreased in the diabetic patients. The frequency of any of these HLA-antigens did not differ in patients with or without diabetic neuropathy. There were no significant differences in the frequencies of insulin antibodies or proliferative responses to insulin antigens between patients with or without diabetic neuropathy. However, patients who were HLA-DR3/DR4 heterozygotes and had diabetic neuropathy responded to insulin antigens more often by proliferation than DR3/DR4 positive patients without diabetic neuropathy. Thus poor glycaemic control is associated with an increased risk for diabetic neuropathy. Patients with DR3/DR4 heterozygocity and failing to respond to insulin antigens by proliferation seem to be less prone to develop diabetic neuropathy.

Adult↗
PubMed2006

Alteration of foot temperature in diabetic neuropathy: is it another piece of puzzle?

Poor glycaemic control and the duration of diabetes mellitus are known to accelerate development and progression of neuropathy. Diabetic co-morbidities: hypertension and hyperlipidaemia, have been postulated to associate with development of neuropathy. A diabetic foot with low temperature and frequent exposure to low temperature environment has recently been hypothesized to be at higher risk to develop early neuropathy. This cross-sectional study is undertaken to identify risk factors for diabetic neuropathy and the association between foot temperature and development of diabetic neuropathy by using simple clinical examination in the outpatient setting. From April 18, to April 30, 2005, universal sampling method was used to select 134 diabetic patients (type 1 or type 2 for >1 year) with peripheral neuropathy. Excluded are those with chronic alcoholism, drug-induced neuropathy, dietary history of vitamin B deficiency and family history of porphyria and hereditary sensorimotor neuropathy. The patient's duration of diabetes, glycaemic control status and the presence of co-morbids: hypertension and hyperlipidemia, were recorded. The temperature of the foot was measured by using thermo buddy. Of 134 patients representing Malaysian ethnic distribution with an equal number of males and females, 20.1% were in the age group of 61 to 65 years and, 85.1% and 67.9% belonged to lower socioeconomic and educational groups respectively. Associations between diabetic neuropathy and glycaemic control (p = 0.018) and duration of diabetes (p < 0.05) were significant. However, hypertension, hyperlipidaemia and low foot temperature were not significantly associated with development of diabetic neuropathy. Poor glycaemic control is significantly associated with diabetic neuropathy. Foot temperature alteration is merely an effect of autonomic neuropathy with a cold foot is attributed to co-existing peripheral arterial disease.

Adult↗
PubMed1999

Autonomic and peripheral (sensorimotor) neuropathy in chronic liver disease: a clinical and electrophysiologic study.

Peripheral neuropathy has been reported in association with chronic liver disease. However, the precise incidence, severity and characteristics of neuropathy, and the relationship of neuropathy to different etiologies of liver disease have not been defined. In this study, 58 patients with advanced liver disease were evaluated in detail for the presence of neuropathy. Peripheral (sensorimotor) neuropathy was found in 71% and autonomic neuropathy was found in 48% of the patients. Although the majority of patients were asymptomatic, neurological examination showed distal sensory loss to pain, or vibration or distal loss of reflexes in 17 patients (29%). Sensory neuropathy was seen more commonly than motor axonal polyneuropathy on nerve conduction studies. Quantitative sensory testing was frequently abnormal (62%) and cooling thresholds were more affected than vibration thresholds. Overall, the pattern of neuropathy in patients with liver disease conformed to the pattern expected in "dying back" or length-dependent neuropathy. The neuropathy was most severe in patients with advanced hepatic decompensation. Comparison of causes of liver disease showed no significant differences in the severity of neuropathy among the different etiologies. In conclusion, axonal sensory-motor polyneuropathy and autonomic neuropathy are commonly seen in patients with end-stage liver disease of different causes.

Adult↗
PubMed2003

Chronic dysimmune neuropathy. A subclassification based upon the clinical features of 102 patients.

The Chronic Dysimmune neuropathies (CDN) are a clinically heterogeneous group of polyneuropathies united by their presumed immune mediated aetiology. At present such neuropathies are classified as Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Multifocal Motor Neuropathy (MMN) and the Neuropathies in association with serum Paraproteins (Paraproteinaemic Neuropathies). This classification fails to recognise other distinctive syndromes and is limited by heterogeneity within, and overlap between, subgroups. We have refined this clinical subclassification by a review of a consecutive series of 102 unselected patients with CDN referred to a single neurologist. We recognise 6 clinical subtypes of CDN: one sensory ataxic group; three motor-sensory subgroups (chronic motor sensory demyelinating neuropathy, subacute motor sensory demyelinating neuropathy and a multifocal motor sensory neuropathy); and two pure motor subgroups (symmetric pure motor demyelinating neuropathy and multifocal motor neuropathy). This subclassification allows distinct syndromes to be recognised and helps resolve problems of heterogeneity and overlap. Distinction between these subgroups is of immediate practical relevance to patient management. Although steroids are beneficial for most of the subgroups, this is not so for both of the pure motor syndromes which should be treated with intravenous immunoglobulin. Patients with chronic development of Motor Sensory Demyelinating Neuropathy respond less well to steroids than those with a subacute onset. An association was found between elderly patients with Subacute Motor Sensory Demyelinating Neuropathy and carcinomas. Within any clinical subgroup patients behave similarly regardless of the presence of associated paraproteins or nerve specific antibodies.

Adolescent↗
PubMed1991

Restoration of blood-nerve barrier in neuropathy is associated with axonal regeneration and remyelination.

We investigated the temporal course of blood-nerve barrier (BNB) breakdown during the evolution of tellurium neuropathy, ricin neuropathy, and Wallerian degeneration following nerve transection or nerve crush. Blood-nerve barrier permeability was assessed with a 4,000-molecular weight fluoresceinated dextran from three days to 19 weeks after onset of neuropathy. Blood-nerve barrier breakdown was present during the first two weeks in all four models of neuropathy. Restoration of the BNB to the dextran began within four weeks and was complete by 14 weeks in tellurium neuropathy, a model of demyelinating neuropathy characterized by rapid remyelination, and after nerve crush, a model of Wallerian degeneration characterized by rapid axonal regeneration into distal stump. In contrast, there was persistence of BNB breakdown beyond 14 weeks in ricin neuropathy, a model of neuropathy with no axonal regeneration or remyelination, and after nerve transection, a model of Wallerian degeneration characterized by minimal axonal regeneration into distal stump. We conclude from these data that alterations in the BNB over the course of neuropathy differ among various types of neuropathy, and that these alterations are dependent on the form of nerve fiber injury. The lack of regenerating or remyelinating axons in ricin neuropathy and after nerve transection may be responsible for the persistent BNB breakdown found in these neuropathies.

Animals↗
PubMed2002

Local sympathetic denervation in painful diabetic neuropathy.

This study assessed whether painful diabetic neuropathy is associated with abnormal sympathetic nervous function in the affected limbs. Nine patients with diabetes (four men, five women; age 61 +/- 7 years) and painful peripheral neuropathy of the feet, but without evidence of generalized autonomic neuropathy, underwent intravenous infusion of tritiated norepinephrine (NE) and sampling of arterial and venous blood in both feet and in one arm to quantify the rate of entry of NE into the local venous plasma (NE spillover). In the same patients, positron emission tomography (PET) scanning after intravenous injection of the sympathoneural imaging agent 6-[(18)F]fluorodopamine was used to visualize sympathetic innervation and after intravenous [(13)N]ammonia to visualize local perfusion. The results were compared with those in the feet of normal volunteers and in an unaffected foot of patients with unilateral complex regional pain syndrome (CRPS). In addition, neurochemical results obtained in painful diabetic neuropathy were compared with those obtained in diabetic control patients with painless neuropathy and diabetic control patients without neuropathy. Local arteriovenous difference in plasma NE levels (DeltaNE(AV)) and NE spillover in the arms did not differ across the groups. However, DeltaNE(AV) in the feet was significantly less in the group with painful diabetic neuropathy than in the control groups. Also NE spillover in the feet tended to be lower in painful neuropathy. DeltaNE(AV) of diabetic control patients without neuropathy (n = 6) resembled values in the control groups without diabetes, whereas patients with painless diabetic neuropathy (n = 6) had evidence suggesting partial loss of sympathetic innervation. PET scanning revealed decreased flow-corrected 6-[(18)F]fluorodopamine-derived radioactivity in patients with painful diabetic neuropathy, compared with values in normal volunteers and patients with CRPS. The results provide neurochemical and neuroimaging evidence for regionally selective sympathetic denervation in the painful feet of patients with diabetic neuropathy.

Aged↗