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PubMed1982

[Peripheral neuropathies. Current data concerning nerve regeneration (author's transl)].

The peripheral neuropathies in humans could be classified both with clinical criteria and pathological aspects. Between these, only axonal neuropathies are subject to regeneration. Axonal neuropathies present two aspects: wallerian degeneration and dying-back neuropathy. Dying-back neuropathy is the commonest type of human neuropathy but wallerian degeneration has been the most studied model of axonal neuropathy. The regeneration in this case lead to two questions: what is the signal for regeneration and what are the factors which improve the nerve growth?

Animals↗
PubMed1984

Dapsone-induced peripheral neuropathy. Case report and review.

A severe motor and a minor sensory neuropathy developed in a man being treated with dapsone (4,4'-diaminodiphenylsulfone) for dermatitis herpetiformis. He had received dapsone for 16 years before any signs of neurotoxicity became evident. Electrodiagnostic and clinical features were consistent with an axonal neuropathy. Clinical characteristics of dapsone-induced neuropathy include a motor neuropathy affecting the extremities, usual onset within five years after the initiation of dapsone therapy, dapsone dosage usually equal to or greater than 300 mg/day, and, almost always, complete recovery from the neuropathy after dapsone-dose reduction or withdrawal. The patient was found to be a slow acetylator of sulfamethazine, and therefore is a slow acetylator of dapsone. An HLA typing was done on the patient. New cases of dapsone-induced neuropathy should be HLA typed and have acetylation profiles in an attempt to identify future high-risk patients. This case is noteworthy for the length of time of dapsone usage (16 years) and the low daily dosage of dapsone (100 mg) taken prior to the development of neuropathy.

Adult↗
PubMed1982

Prednisone-responsive hereditary motor and sensory neuropathy.

Neurologic improvement with use of prednisone, in some cases on several occasions, was demonstrated in seven patients who had a chronic progressive polyradiculoneuropathy with nerve conduction velocity and electromyographic findings consistent with segmental demyelination and axonal degeneration and increases protein concentration in the cerebrospinal fluid. These patients seemed to have the progressive form of chronic inflammatory-demyelinating polyradiculoneuropathy and, in addition, had clinical features of hereditary motor and sensory neuropathy including pes cavus and hammer toes. On systematic examination, bony abnormalities or asymptomatic neuropathy typical of subclinical inherited neuropathy was discovered among their kin. There patients might therefore be identified as having inflammatory-demyelinating hereditary motor and sensory neuropathy. These cases may represent a chance association of chronic inflammatory-demyelinating polyradiculoneuropathy and hereditary motor and sensory neuropathy, a causally linked association of these disorders, or a prednisone-responsive inherited neuropathy only. We wish to draw attention to this treatable neuropathy and to raise the question of whether environmental factors play role in the expression of dominantly inherited mutant genes.

Adolescent↗
PubMed1995

[Value of proximal conduction block study in diagnosis of inflammatory neuropathies].

Conduction block is a common finding in inflammatory neuropathies, indicating circumscribed demyelination. Since demyelination and conduction block are often localized proximally, the whole ulnar nerve including its proximal segments was studied fractionally in 31 patients with inflammatory neuropathies. In 5 of 15 patients with Guillain-Barré syndrome, conduction block at the spinal roots was the first electrophysiological finding indicating demyelinating neuropathy. Segmental conduction blocks were also found in 8 of 9 patients with chronic inflammatory demyelinating polyneuropathies (CIDP) and 4 of 4 patients with atypical neuropathies. In 3 patients, multifocal motor neuropathy (MMN) could only be differentiated from motor neuron disease by recording proximal conduction block. Corresponding to clinical recovery, conduction block improved with immunoglobulin therapy in CIDP and MMN patients. The technique of proximal conduction block studies clearly improves the diagnosis of focal demyelination in inflammatory, treatable neuropathies. They should be performed particularly in patients with atypical neuropathies in whom electrophysiological tests of distal nerve segments show normal results.

Adolescent↗
PubMed1994

[Clinical factors relating to the presence of serum anti-GM1 and GD1b antibodies in demyelinating neuropathy--study using a multivariate analysis].

We studied clinical factors relating to the presence of serum anti-GM1 and GD1b antibodies in patients with demyelinating neuropathy using a multivariate analysis. Sera were obtained from 46 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and 33 with Guillain-Barré syndrome (GBS) and kept frozen at -20 degrees C until use. Anti-GM1 and GD1b IgM and IgG antibodies were measured by ELISA at serum dilution of 1:100 and considered to be positive when those values were more than the cut off values determined by means and standard deviations in 35 normal controls. Age, sex, duration, prodromal disease, neurological findings, concentration of CSF protein, nerve conduction, treatment, and outcome were investigated in all patients retrospectively. Multivariate logistic models using all those characteristics were used to clarify the clinical factors relating to the presence of anti-GM1 and GD1b antibodies. In CIDP, anti-GM1 antibodies associated with or without anti-GD1b antibodies were frequently seen in patients with motor dominant neuropathy than those with sensory dominant neuropathy (P = 0.007, odds ratio = 11.6). There was significant difference in anti-GM1 IgM antibodies (P = 0.003, odds ratio = 22.2), but no difference in IgG antibodies. Anti-GM1 antibodies were observed 5 (IgM, 5; IgG, 2) of 7 patients with pure motor neuropathy, 9 (IgM, 8; IgG, 4) of 17 with motor dominant neuropathy, 5 (IgM, 2; IgG, 3) of 16 with sensori-motor neuropathy, and none of 6 with sensory dominant neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Long-term neuropathy after regional isolated perfusion with melphalan for melanoma of the limbs.

The incidence of long-term (> or = 3 months) neuropathy in 350 melanoma patients treated with single normothermic or 'mild' hyperthermic perfusion with melphalan in the period 1978 to 1990 was studied. Long-term neuropathy was encountered in 14 patients; in 10/51 patients (20%) after perfusion at the axillary level and in 4/247 patients (2%) after perfusion at the iliac level. After brachial and femoro-popliteal perfusions no long-term neuropathy was observed. Neuropathy, mainly consisting of paresis/paralysis of the hand and/or fingers, anaesthesia, and/or paraesthesiae, improved over a mean period of 16 (3-43) months in eight patients, but three patients still had serious neuropathy one year after perfusion. In another six patients little improvement was seen and four died with permanent neuropathy. Acute regional toxicity after perfusion and the application of 'mild' hyperthermia did not seem to influence the incidence of long-term neuropathy. This complication is probably a result of the isolating Esmarch rubber bandage being applied too tightly during perfusion at a proximal level. At the axillary level, where the brachial plexus lacks the protection from enveloping tissues, nerve damage is especially prone to occur. We recommend applying this bandage no tighter than is necessary to maintain the isolation of the circuit. This implies meticulous surgical isolation of the vascular system and accurate monitoring of leakage.

Adolescent↗
PubMed1995

[Sensory ataxic neuropathy associated with Sjögren's syndrome].

One tenth of patients with Sjögren's syndrome (SS) is associated with peripheral neuropathy. Trigeminal neuropathy, mononeuropathy multiplex, sensory neuropathy, distal sensory neuropathy, ataxic sensory-autonomic neuropathy have been described as the neuropathy associated with SS. However, some of them secondary occur associated with the vasculopathy due to rheumatoid arthritis, systemic lupus erythematodes etc combined with SS. We demonstrated the clinico-patho-physiological features and spinal MRI findings of patients with primary SS in whom the sensory ataxia and autonomic dysfunctions were the predominant symptoms. The underlying pathology was lymphocytic (T cells) infiltration to the dorsal root ganglia with sensory neuronal degeneration. These findings have identified as association between SS and sensory ataxic neuropathy.

Aged↗
PubMed1996

[Axial and para-axial fluorophotometry in optic neuropathies].

PURPOSE: To investigate optic neuropathies, with normal results in fluorescein fundus angiography, by axial and paraaxial fluorophotometry (a type of topographic vitreous fluorophotometry) in order to determine differences examined in the amount of fluorescein leakage in macular and optic disc. MATERIAL AND METHODS: We studied 12 eyes with unilateral idiopathic retrobulbar inflammatory optic neuropathy and 4 eyes with unilateral posterior ischaemic optic neuropathy during the acute phase: control group consisted of 5 healthy eyes. After 3-4 months, in final stage of optic neuropathies, in which primary atrophy of optic disc developed (6 eyes), fluorophotometric examinations were repeated. All cases of control group underwent axial and paraaxial fluorophotometry. Complete ophthalmic, physical and neurological examinations were performed. RESULTS: The mean fluorophotometric values of PVPR (posterior vitreous penetratio-ratio) for f-scans (foveal) were lower than for t-scans (PVPRf < PVPRt) in all neuropathies during the acute phase but all values of PVPR were higher than in control eyes. In late phase of the neuropathies in which primary atrophy of optic disc developed we found a trend: PVPRt < PVPRf, but all values of PVPR were lower than in control eyes. We noticed increased permeability of the blood-ocular barrier and difference between fluorophotometric readings for optic disc directions (t-paraaxial scans) and for foveal directions (f-axial scans) in optic neuropathies during the acute phase, when the findings on ophthalmoscopic and fluorescein fundus angiography were normal.

Adult↗
PubMedDate not supplied

[Risk factors in the epidemic neuropathy of Cuba].

OBJECTIVE: A case control study to find out if Cuba's epidemic neuropathy was a result of one of the following causes: (1) an infectious process, (2) exposure to one or more toxical agents, (3) low intake of one or more nutrients, or (4) more than one of such causes and their interactions. MATERIAL AND METHODS: A total of 311 cases of epidemic neuropathy with optic and peripheral symptoms and 377 controls were studied. A questionnaire with 55 items was employed to document exposure to factors determined by the etiologic hypothesis. Data analysis was done separately for the optical and peripheral types of the disease. RESULTS: No association was found between illness and any deficiency of basic sanitation for both types of neuropathy. Acute stress, irregularities in food intake, body weight loss in the last 12 months and other indicators of nutritional deficiencies were associated to both clinical manifestations, although they were also high in the controls. Low frequency of illness was found for people living with diseased persons. Females had a significant high risk of illness in the peripheral manifestations whereas smoking was the only toxical risk factor in optical neuropathy. Nutritional deficiencies together with unidentified personal factors were the main associations for illness outcome; smoking increased significantly the risk of optical neuropathy. CONCLUSIONS: 1. The infection etiology was unsupported in the study. 2. Smoking appeared as a factor for the optical neuropathy. 3. Stress induced by vital events were significantly associated with the disease. 4. Both types of the neuropathy were associated to body weight loss and other indicators of nutritional deficit.

Case-Control Studies↗
PubMed1998

High prevalence of peripheral neuropathy in hepatitis C virus infected patients with symptomatic and asymptomatic cryoglobulinaemia.

BACKGROUND: Fifty per cent of patients with chronic hepatitis C, show detectable cryoglobulinaemia, even though most of them do not show cryoglobulinaemia related symptoms. Peripheral neuropathy is present in most of the patients with symptomatic cryoglobulinaemia, where it may be the first clinical manifestation. The prevalence of peripheral neuropathy in patients with hepatitis C and cryoglobulinaemia is unknown. AIMS: To assess the prevalence of peripheral neuropathy in HCV infected patients with symptomatic or asymptomatic detectable cryoglobulinaemia. PATIENTS AND METHODS: Eighty-nine patients with HCV infection and detectable cryoglobulinaemia underwent electrophysiological studies. RESULTS: Electrophysiological evidence of peripheral neuropathy was found in 37% and was significantly associated with: the presence of cryoglobulinaemia syndrome, older age, higher rheumatoid factor reactivity and immunoglobulin M levels and reduced complement C4 activity. However, electrophysiological evidence of peripheral neuropathy was unrelated to cryocrit levels and type of cryoglobulinaemia and was found in 23/68 patients without any symptoms of cryoglobulinaemia other than pain and paresthesia. CONCLUSIONS: These findings suggest that peripheral neuropathy is frequent in patients with hepatitis C and detectable cryoglobulins. Neuropathy was found to be present in 1/3 of patients without other cryoglobulinaemia-related symptoms, thus a direct or indirect role of HCV, independent of cryoglobulinaemia, in the pathogenesis of nerve damage cannot be ruled out.

Age Factors↗
PubMed1998

Genetically determined neuropathies.

There have been major advances in the understanding of the genetically determined neuropathies in recent years. The underlying genetic defects are now known for many of the demyelinating hereditary motor and sensory neuropathies, and linkage data are available for some of the axonal hereditary motor and sensory neuropathies. This has important implications for both diagnosis and genetic counselling in this group of conditions. The genetic defect in most cases of familial amyloid polyneuropathy is also now known. In the most common form of familial amyloid polyneuropathy (FAP), transthyretin-related FAP, liver transplantation has been established as the first definitive treatment for a hereditary neuropathy and should be considered especially in young adult patients. This review will concentrate on the advances in the molecular genetics of the hereditary motor and sensory neuropathies, the hereditary sensory and autonomic neuropathies and the familial amyloid polyneuropathies with particular emphasis on the difficulties in classifying the first group.

Adult↗
PubMed2001

Electrophysiological course of uraemic neuropathy in haemodialysis patients.

The objective of this study was to confirm electrophysiologically both the presence and course of uraemic neuropathy in haemodialysis patients. Nerve conduction studies of the lower extremities were done in 70 haemodialysis patients and 20 normal volunteers. Compared with that in normal volunteers, the distal motor latency in the tibial nerve of patients was prolonged significantly (p<0.05), and the minimal F wave latency in the tibial nerve was also prolonged significantly (p<0.05). Motor conduction velocity in the tibial nerve was reduced significantly (p<0.05), and sensory nerve conduction velocity in the medial plantar nerve also was reduced significantly (p<0.05). These results suggest the presence of uraemic neuropathy in haemodialysis patients. Twenty patients were investigated by a follow up study five years later. Parameters from F wave conduction studies, which were thought to be the most useful in the evaluation of neuropathy, showed no significant differences between the initial and follow up trials. These observations suggest that uraemic neuropathy does not progress during haemodialysis. These results also suggest that most haemodialysis patients showed electrophysiological evidence of uraemic neuropathy, but no remarkable electrophysiological change in uraemic neuropathy during haemodialysis was recognised.

Adult↗
PubMedDate not supplied

[Advances in the molecular genetics of the hereditary neuropathies].

OBJECTIVE: We reviewed current knowledge of the molecular and genetic bases of hereditary peripheral neuropathies, with special emphasis on the senso motor neuropathies and their different clinical phenotypes. DEVELOPMENT: The peripheral neuropathies show great clinical variability and genetic heterogeneity. To date 12 genes and over 20 genetic loci have been described in relation to Charcot Marie Tooth disease and related neuropathies. The commonest form is the type 1A Charcot Marie Tooth disease (CMT1A) caused by tandem duplication of a monomer of 1.5 megabases (Mb) on chromosome 17q11.2. The CMT 1A duplication is found in 70% of the patients with CMT 1. The deletion of 1.5 Mb is the most prevalent mutation (85%) in hereditary neuropathy with susceptibility to paralysis due to pressure. This monomer includes the PMP22 gene which is affected by a genetic dose effect. The different proteins encoded by the genes described are well expressed in the Schwann cell and in the nerve axon. They have different functions. There are the structural proteins of myelin, transcription factors, cytoskeleton components, molecular motors of the microtubules, proteins involved in growth and cellular differentiation or with presumed enzyme activity. CONCLUSIONS: Diagnosis of molecular pathology is important for genetic counselling. The development of new treatment for hereditary neuropathies is based on the generation of animal models for the different genes and on understanding the role of the proteins involved in axon Schwann cell interaction.

Animals↗
PubMed1996

Cardiovascular, metabolic, and hormonal responses to noradrenaline in diabetic patients with autonomic neuropathy.

Denervation hypersensitivity is a well-known phenomenon in patients with autonomic failure. In diabetic autonomic neuropathy hypersensitivity to beta-adrenergic stimulation has been demonstrated. We infused noradrenaline, mainly an alpha-adrenoceptor agonist, in three escalating doses (0.5, 2.5, and 5 micrograms min-1) in three age and sex matched groups of eight subjects: healthy volunteers, diabetic patients with and without autonomic neuropathy. During steady state in each infusion period we measured heart rate, blood pressure, cardiac output, hepato-splanchnic blood flow, vascular resistance, glucose kinetics, metabolites (beta-hydroxybuturate, glycerol, and lactate), and glucoregulatory hormones (noradrenaline, adrenaline, growth hormone, pancreatic polypeptide, cortisol, and insulin). Systolic and mean blood pressure increased in all groups but diabetic patients with autonomic neuropathy showed a significantly higher increase (p < 0.01) than the other two groups, with a lower threshold for increase in blood pressure. Cardiac output, hepato-splanchnic blood flow, vascular resistance, and heart rate did not change in any of the groups. The incremental increase in glucose and beta-hydroxybuturate was higher in patients with autonomic neuropathy. Otherwise, only minor changes were seen in hormonal and metabolic parameters. The cardiovascular hypersensitivity seen in diabetic autonomic neuropathy was mainly explained by increased peripheral vascular resistance, which increased significantly (p < 0.05) more in these patients. In conclusion, diabetic patients with autonomic neuropathy show denervation hypersensitivity to alpha-adrenergic stimulation by noradrenaline, especially as regards cardiovascular effects.

3-Hydroxybutyric Acid↗
PubMed1998

Lowering the risk of neuropathy, foot ulcers and amputations.

Peripheral neuropathy is one of the most common long-term complications of Type 2 diabetes. A population-based study in the north of England showed that 42% of Type 2 diabetic patients had clinical evidence of neuropathy. The Diabetes Control and Complications Trial (DCCT) has shown that the incidence of neuropathy in Type 1 diabetes can be reduced by over 50% with intensive therapy and optimal glycaemic control. Hyperglycaemia is believed to be a major aetiological factor in the development of neuropathy in Type 2 diabetes. Neuropathy cannot be diagnosed through history alone; therefore, careful examination of the feet for evidence of sensory loss and an assessment of the circulation must form part of the annual review of each patient. Peripheral somatic and autonomic neuropathy, together with peripheral vascular disease, are major contributing factors to the development of foot ulcers. In addition, abnormalities of foot shape (e.g. claw toes, prominent metatarsal heads) and the presence of plantar callus are signs of foot-ulcer risk. Effective patient education can reduce the incidence of foot ulceration and amputation by over 50%; therefore, all patients with a high risk of foot ulcers should be informed and, if indicated, referred for regular podiatry. The team approach to diabetic foot problems is an effective method of providing treatment for active ulcers. This should be followed by appropriate education, the provision of follow up and if indicated, suitable footwear and hosiery. Key members of the team are the podiatrist, the specialist nurse and the orthotist; medical staff may include the diabetologist and a vascular or orthopaedic surgeon. Thus, the risk of foot ulceration and amputation can be reduced by careful screening and patient education, without the need for expensive equipment.

Amputation, Surgical↗
PubMed2000

Surgery for nonarteritic anterior ischemic optic neuropathy.

BACKGROUND: Nonarteritic ischemic optic neuropathy is characterized by sudden and painless loss of vision in one eye, accompanied by pallid swelling of the optic disc. Although various medical interventions, such as corticosteroids and phenytoin sodium, have been used to treat nonarteritic ischemic optic neuropathy, no therapy has been proven effective. OBJECTIVES: The objective of this review is to assess the safety and efficacy of surgical treatment compared with other treatment or usual care in people with nonarteritic ischemic optic neuropathy. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register - Central and MEDLINE. The most recent searches were performed in December 1997. SELECTION CRITERIA: We included randomized trials comparing surgery to no surgery in people with nonarteritic ischemic optic neuropathy. DATA COLLECTION AND ANALYSIS: We obtained full copies of all potentially relevant articles. Only one article described a randomized trial of surgery and it was eligible for inclusion. No formal assessment of quality was done. One reviewer extracted data. No synthesis was required, as there was only one trial. MAIN RESULTS: The one trial identified randomized 258 patients. The only published report with outcomes data for that trial presents preliminary results from 244 patients who had achieved six months of follow-up at the time of the report. Participants assigned to surgery did no better than participants assigned to careful follow-up regarding improved visual acuity of three or more lines of vision at six months: 32.6% of the surgery group improved compared with 42.7% of the careful follow-up group. The adjusted odds ratio (OR), adjusted for baseline visual acuity and diabetes, comparing the two groups for three or more lines improvement was 0.74 (95% confidence interval (CI) 0.39 to 1. 38) (surgery group improvement was worse than careful follow-up). In addition, participants receiving surgery had a significantly greater risk of losing three or more lines of vision at six months: 23.9% in the surgery group worsened compared with 12.4% in the careful follow-up group. The six-month adjusted OR comparing the two groups for loss of three or more lines of vision was 1.96 (95% CI 0.87 to 4.41). Spontaneous improvement of three or more lines of vision was observed in 42.7% of participants in the careful follow-up group. REVIEWER'S CONCLUSIONS: Results from the Ischemic Optic Neuropathy Decompression Trial indicate that optic nerve decompression surgery for nonarteritic ischemic optic neuropathy is not effective.

Humans↗
PubMed1996

Neurotrophic factors in the treatment of peripheral neuropathy.

Peripheral neuropathies are common and frequently debilitating disorders which may include various subpopulations of motor, sensory or autonomic neurons depending on the underlying aetiology. They are likely to be the first group of neurological disorders to be successfully treated with growth factors since peripheral nerves are accessible to proteins given systemically. Preclinical and ongoing clinical trials of nerve growth factor (NGF) suggest that it will be useful for the treatment of diabetic, toxic and compressive sensory neuropathies. At appropriate doses NGF has no significant side effects in humans. Since NGF administration to mature animals stimulates synthesis of brain-derived neurotrophic factor and perhaps other neurotrophins in peripheral nerves, the spectrum of neuropathies treatable with NGF is wider than might be predicted. Preclinical studies suggest that insulin-like growth factor 1 (IGF-1) will be useful for the treatment of mixed motor and sensory neuropathies. For example, IGF-1 treatment can prevent the experimental motor and sensory neuropathies caused by the antitumour drugs, vincristine and cisplatin. Other neurotrophic factors have also shown promise in preclinical trials. The successful use of growth factors in the treatment of peripheral neuropathies may provide the first true therapy for this previously untreatable and devastating group of neurological disorders.

Animals↗
PubMed1993

Sixteenth annual AAEM Edward H. Lambert Lecture. Electrodiagnostic aspects of diabetic neuropathies: entrapments. American Association of Electrodiagnostic Medicine.

A MEDLINE review suggested a lack of recent studies about the entrapments seen with underlying diabetic neuropathy. Suggested protocols for research in diabetic peripheral neuropathy have not included the concepts of entrapments as an early--indeed, first manifestation of the neuropathy. Carpal tunnel syndrome is a frequent accompaniment of diabetic peripheral neuropathy. Assessment of the degree of entrapment superimposed on the generalized peripheral neuropathy can be clarified by analysis of the CMAP and the SNAP--particularly with respect to duration of the negative spike of the action potential. Also, analysis of the action potentials elicited by stimulation of the ulnar and radial nerves and their comparison with the median nerve is often helpful. Finally careful inspection of the action potential when stimulating proximal and distal to the entrapment will establish the degree of nerve compromise relative to the underlying diabetic neuropathy.

Action Potentials↗