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PubMed1982

[Neurotoxic substances as a tool to understand some mechanisms of peripheral neuropathies (author's transl)].

The study of toxic experimental models of neuropathies has been a decisive step to understand some cellular mechanisms of human neuropathies. The progressive development of toxic neuropathies allow to the possibility of isolating their initial mechanism. Dying back axonopathies are the commonest neuropathies as observed in clinical practice, and their experimental models had been extensively studied. Acrylamide and n-hexane intoxications have shown the following results : 1) The onset of the neuropathy is located at the most distal node of the longest and largest fibres. Sensory fibres are impaired before the motor ones. 2) Fast axoplasmic transport stops distally. 3) Impaired enzymes of the energetic cycle were observed distally. Proximal axonopathies as those resulting from IDPN intoxication are a possible model to clear up the cellular mechanisms of the lateral amyotrophic sclerosis. Human toxic neuronopathies and myelinopathies are uncommon. Such experimental models are described in relation to other human neuropathies.

Acrylamides↗
PubMed1981

[Neuropathy in angioimmunoblastic lymphadenopathy (author's transl)].

Four cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy are described. The neuropathy was mixed, sensory and motor, more or less extensive, always asymetrical. In two cases, the clinical symptomatology and the clinical course were very peculiar, characterized by sensory disorders of a precise topography, circumscribed and sometimes suspended and by a relapsing and remitting course. In the third case, the neurological signs were acute and rapidly extensive with mandatory respiratory assistance. In this case, death occurred after a few weeks and the exact diagnosis was only attained at post-mortem examination. In the fourth case the neuropathy was very painful but the course was slow. In all four cases marked and extensive pain was present prior to the neurological disorders. Electrophysiological abnormalities were a constant feature with a marked slowing down of nerve conduction velocity. CSF was normal at the beginning in one case but was otherwise markedly pathological with an increased number of cells due to a large number of lymphocytes ranging from 6 to 40 cells while protein ranged from 60 to 160 mg per 100 ml. Nerve and muscle biopsies were non specific, i.e. neurogenous muscular atrophy and demyelination, except in case n. 4 where specific angioimmunoblastic lymphadenopathy infiltrates were present both in nerve and muscle. In cases 1 and 3 a non specific lymphohistiocytic infiltrate was present in spinal roots and meninges. Corticotherapy was used and efficient in two cases. These data are compared with a review of the literature. Since 1976, 7 cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy have been reported. Clinical, electrophysiological and biological features are similar. Only one case underwent a post mortem examination of the central nervous system: a non specific lymphocytic infiltration in the spinal roots and meninges was mentioned. The role of the dysproteinemia associated with the AIL in the occurrence of the neuropathies is discussed. It remains a possible factor only. The role of a massive specific localization of the pathological process is well established in only one case (case 4). Such localization in lymphomas are not unusual. In 2 of our cases as well as in 2 from the literature the pathological findings are non specific: mild lymphoplasmocytic infiltrates of spinal roots and meninges. Those lesions are similar to neuropathies associated to non metastasizing neoplasms or malignant hemopathies.

Aged↗
PubMedDate not supplied

Neuropathies associated with monoclonal gammapathies.

There is increasing evidence that monoclonal proteins are implicated in the development of peripheral neuropathy. Approximately ten percent of patients with peripheral neuropathy of unknown cause have a monoclonal protein and this rate is significantly higher than prevalence rates of monoclonal protein in comparable segments of the general population. Extensive clinical, electrophysiological and immunopathological evidences indicate that peripheral neuropathy associated with monoclonal protein are heterogeneous, including: 1. the demyelinating, predominantly sensory neuropathies associated with anti-MAG antibodies; 2. the axonal, sensory neuropathies associated with anti-sulfatide and anti-chondroitin sulfate antibodies; 3. the motor neuropathies associated with anti-GM1 antibodies. Patients with chronic polyneuropathies should be evaluated for underlying plasma cell dyscrasia.

Adult↗
PubMed1994

Cuban epidemic optic neuropathy. Mitochondrial DNA analysis.

OBJECTIVE: To search for mitochondrial DNA (mtDNA) mutations previously associated with Leber's hereditary optic neuropathy (LHON) in patients with an optic neuropathy that appeared in epidemic form in Cuba. METHODS: Twelve Cuban patients underwent a comprehensive neuro-ophthalmologic examination and were found to have a characteristic optic neuropathy, Cuban epidemic optic neuropathy (CEON). At the same time, one patient was diagnosed with typical LHON that occurred during the epidemic. Blood samples were taken from these patients as well as from 3 controls with normal neuro-ophthalmologic examinations. These samples were blindly analyzed for 9 LHON-associated mtDNA mutations by molecular genetic methods. RESULTS: CEON bore clinical and epidemiological similarity to LHON, however, family histories, systemic symptoms (especially weight loss and polyuria), and symptoms of peripheral neuropathy permitted a clinical distinction. None of the 12 patients with CEON or 3 controls had any of the LHON-associated mtDNA mutations. Only the patient with clinical LHON, who did not meet the case definition for CEON, harbored the 11778 mtDNA mutation. CONCLUSIONS: Known mtDNA mutations are not found frequently in CEON patients but they may contribute to some cases of Cuban optic neuropathy. CEON may represent an acquired variety of mitochondrial dysfunction induced by nutritional deficiencies, toxins, or both. Alternatively, CEON patients may also harbor as yet undiscovered mtDNA mutations that contribute to their genetic susceptibility.

Cuba↗
PubMed1994

Vasculitic neuropathy.

Patients with vasculitic neuropathy may present with either mononeuritis multiplex, or a symmetrical or asymmetrical sensorimotor neuropathy. In those patients whose neuropathy is part of a systemic vasculitis the neuropathy can be expected to improve leaving only mild or moderate functional disability. Nevertheless, the long-term outlook for such patients is poor with a 5-year survival of around 50% with most excess deaths being due to vascular disease. The prognosis in non-systemic vasculitic neuropathy is almost certainly substantially better than this. Treatment of vasculitic neuropathy should be based on diagnosis by tissue biopsy, usually of nerve, and early use of aggressive immunosuppression.

Autoimmune Diseases↗
PubMed1994

Inherited neuropathies: Charcot-Marie-Tooth disease and related disorders.

Collectively, the inherited disorders of peripheral nerves represent a common group of neurological diseases and are frequently encountered in the clinical setting. Recent advances in molecular genetics have not only provided improved diagnosis and counselling, but may ultimately lead to specific, rational therapies for the various forms of inherited neuropathy. Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a genetically heterogeneous group of chronic demyelinating polyneuropathies with loci mapping to chromosome 17p (CMT1A), chromosome 1q (CMT1B), the X chromosome (CMTX) and to another unknown autosome (CMT1C). CMT1A is most often associated with a tandem 1.5-megabase (Mb) duplication in chromosome 17p11.2-12, or may occasionally result from a point mutation in the peripheral myelin protein 22 (PMP22) gene. CMT1B is associated with point mutations in the myelin protein zero (P0) gene. The molecular defect in CMT1C is unknown. CMTX is associated with defects in the connexin 32 gene. Charcot-Marie-Tooth neuropathy type 2 (CMT2) is an axonal neuropathy, also of undetermined cause. One locus for CMT2 has been assigned for chromosome 1p (CMT2A). Dejerine-Sottas disease is a severe, infantile-onset, demyelinating polyneuropathy which may be associated with point mutations in the P0 or PMP22 genes. Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder that results in a recurrent, episodic demyelinating neuropathy. HNPP is associated with a 1.5-Mb deletion in chromosome 17p11.2-12 and may result from reduced expression of the PMP22 gene. CMT1A and HNPP are apparent reciprocal duplication/deletion syndromes originating from unequal cross-over during germ-cell meiosis.

Charcot-Marie-Tooth Disease↗
PubMed1996

A catechol derivative (4-methylcatechol) accelerates the recovery from experimental acrylamide-induced neuropathy.

Acrylamide (ACR) monomer produces neuropathy of the dying-back type and 4-methylcatechol (4-MC) is a potent stimulator of endogenous nerve growth factor synthesis. In the present study, we investigated the efficacy of 4-MC in promoting recovery from experimental ACR neuropathy in rats. Twenty-two Sprague-Dawley rats were made neuropathic by ACR injections. They showed hindlimb paralysis, increment of landing foot spread distance and a statistically significant reduction in motor nerve conduction velocity. After the ACR neuropathy had been established, 12 of the rats were administered 4-MC for 2 weeks, and the other 10 were injected with phosphate-buffered saline alone. 4-MC-administered ACR neuropathy rats showed improvement, i.e., a decrease in landing foot spread distance, increase in motor nerve conduction velocity and increase in nerve growth factor content in the sciatic nerves in comparison with the corresponding values for ACR neuropathy rats given phosphate-buffered saline alone. A decreased number of large myelinated fiber with a reciprocal increase in small myelinated fiber number also was seen in the ACR neuropathy rats; however, this change was ameliorated in part by the administration of 4-MC. Therefore, these findings suggest that 4-MC can accelerate the recovery process clinically, electrophysiologically, biochemically and neuropathologically.

Acrylamides↗
PubMed1995

Parental history of alcoholism: a risk factor for alcohol-related peripheral neuropathies.

The aim of this study was to identify the risk factors of alcohol-related peripheral neuropathies. A case-control study was performed to compare two groups of alcoholic patients, one with peripheral neuropathy and the other without, but with alcohol-related cirrhosis, pancreatitis or cardiomyopathy. Ninety patients were recruited in four in-patient units of a French hospital: 32 patients had a peripheral neuropathy and 58 patients did not. Univariate analysis showed no differences between the two groups for sex, age, body mass index and duration of the alcoholic disease. Peripheral neuropathies were associated with a higher frequency of parental history of alcoholism, severity of alcohol dependence, heavier alcohol consumption and more alcohol-related somatic diseases. Multivariate analysis showed a strong relationship between a parental history of alcoholism and the presence of a neuropathy, when the severity of the alcoholic disease was taken into account (adjusted OR = 6.8, IC95% [2.2-21.6], P < 0.001). The hypothesis that neuropathy may be a marker of an inherited susceptibility to alcoholism is discussed.

Adult↗
PubMed1996

Immune neuropathies in childhood.

In contradistinction to older populations, immune-mediated disorders (principally demyelinating processes) account for nearly half of peripheral neuropathies in childhood. The largest single diagnostic entity is GBS, which makes up approximately 25% of sensorimotor neuropathies in patients under 18 years of age. The clinical features are similar to those encountered in adults, although the prognosis in youngsters appears to be better than in older populations. Despite the absence of prospective data, plasmapheresis seems to be an effective modality for hastening recovery during GBS in children. The use of human immunoglobulin has gained acceptance for the treatment of GBS in adults, but insufficient data exist to draw firm conclusions about it role in the management of paediatric GBS. CIDP is the second most common cause of chronic sensorimotor neuropathy in children. The clinical manifestations of this disorder are extremely variable, and it can mimic the phenotype of several genetically determined neuropathies. The prognosis in this disorder is also relatively good, although a small number of children have significant neurological disability or treatment side-effects. Other immune-mediated neuropathies are relatively infrequent in our experience. When they occur, they are often associated with collagen-vascular diseases or bone marrow transplantation. Peripheral neuropathy in association with HIV infection in children appears to be rare.

Adolescent↗
PubMed1996

Molecular pathogenesis of peripheral neuropathy.

Peripheral neuropathies can result from a failure to form or maintain the myelin internode or from autoimmune-mediated demyelination. Several gene defects responsible for the most common inherited human peripheral neuropathies referred to as Charcot-Marie-Tooth disease have been reported. These studies identified PMP-22 and connexin-32 as proteins that are essentiel for normal myelination. Point mutations in Po protein, PMP-22, and connexin-32 have been identified as causes of inherited peripheral neuropathies. In addition, studies indicated for the first time that alterations in PMP-22 gene dosage (trisomy and monosomy) can induce inherited peripheral neuropathies. Little is known, however, about how these gene defects cause myelin pathology. This report describes the distributions of proteins within the peripheral myelin internode and discusses how these molecules contribute to the pathogenesis of inherited and autoimmune peripheral neuropathy. A better understanding of the molecular composition of the myelin internode is essential for diagnosis and treatment of human peripheral neuropathies.

Autoimmune Diseases↗
PubMed1996

Peripheral neuropathy in AIDS patients at Kenyatta National Hospital.

Between June and December 1992 forty AIDS patients as defined by the CDC criteria, admitted to the medical wards of the Kenyatta National Hospital, were studied to determine the prevalence and pattern of peripheral neuropathy. Their mean age was 33 +/- 3 years with a range of 16 to 55 years. Clinical and laboratory assessment were carried out both to confirm peripheral neuropathy and exclude other causes of peripheral neuropathy apart from AIDS. All the patients had nerve conduction and electromyographic studies done. Eighteen patients were asymptomatic while fourteen had both signs and symptoms. The commonest symptom was painful paresthesiae of the limbs (35%) while the commonest sign was loss of vibration sense (60%). When symptoms, signs, and electrophysiological studies were combined, all the patients fitted the definition of peripheral neuropathy. The commonest type of peripheral neuropathy was distal symmetrical peripheral neuropathy (DSPN) (37.5%).

Acquired Immunodeficiency Syndrome↗
PubMed1996

Isolated triceps weakness in exercise-induced radial neuropathy.

OBJECTIVE: We report a case of isolated triceps weakness resulting from radial neuropathy. PATIENT: A middle-aged healthy man, a keen athlete, developed acute weakness of the triceps brachii muscle due to radial neuropathy. No other radial nerve innervated muscles were involved. Triceps function completely recovered in six weeks clinically and electrophysiologically suggesting focal conduction block secondary to demyelination. DISCUSSION: Acute radial neuropathy after strenuous arm exercise resulting from a compression lesion with acute conduction block, has been previously described. However, all reported cases involved severe weakness of radial nerve innervated distal muscles with wrist drop, while isolated weakness of the triceps brachii muscle in radial neuropathy has never been previously described. CONCLUSIONS: We suggest that selective weakness in the triceps could be the sole manifestation of an exercise-related radial neuropathy. This particular type of radial neuropathy could be a variant of neuralgic amyotrophy.

Action Potentials↗
PubMed1997

[Non-uremic neuropathy in hemodialysis patients].

We have reviewed 20 clinical records of hemodialysis patients with neuropathy admitted to the Department of Neurology during 1978 april through 1995 march. The clinical diagnosis was made based on clinical findings, neurophysiological examinations, and histopathological findings of sural nerve and peroneal muscle biopsies. Four out of twenty hemodialysis patients with neuropathy were non-uremic neuropathy. The diagnosis of neuropathy of four patients were chronic inflammatory demyelinating polyneuropathy, neuropathy with graft versus host disease, Guillain-Barré syndrome, and subacute combined degeneration of the spinal cord. All patients improved after the treatment. It is important to consider the possibility of association of non-uremic neuropathy in hemodialysis patients.

Adult↗
PubMed1997

[Clinical characteristics of the peripheral form of epidemic neuropathy in the province of Cienfuegos].

INTRODUCTION: From October 1992 to September 1993 clinical observations of the civil population of Cienfuegos revealed the presence of epidemic neuropathy (EN) reaching about 2,000 patients. The clinical manifestations were not uniform. Although numerous studies have been carried out in our country, none have established the characteristics of EN 'the peripheral form'. MATERIAL AND METHODS: We studied the first 50 patients assisted by the neurological services of the clinical surgical hospital Dr. Gustavo Aldereguia Lima of Cienfuegos diagnosed of EN 'peripheral form' according to the procedure established by Ministry of Public Health of Cuba. A clinical history was made for each patient consisting of: General data, history of toxic, nutritional, malabsorption factors and chronic illnesses; symptoms and a neurological examinations. Laboratory test, in a group of patients, were done in sera, urine, cerebrospinal fluid (CSF), gastric juice and neurophysiological studies that included computerized evoked potentials and electroencephalograms registers. RESULTS: Upon analysis of the clinical history, nutritional factors was common to all the patients associated to toxic and malabsorption. The clinical forms were neuropathy (NP) 48%, myeloneuropathy (MNP) 42% and myelopathy (MP) 10%. Retrobulbar optic neuropathy was observed in 42% of the patients and auditory neuropathy in 22%. CONCLUSIONS: The clinical characteristics of NP, in our cases, indicated that this disease fundamentally affects the sensorial neurons and the sensitive peripheral nerves, bilaterally, symmetrically, distally and predominantly in lower limbs. The pathological process has been associated with a distal axonopathy. However, clinic signs of myelopathy can be found up to 40% frequently combined with neuropathy or in isolated form, and seems to affect the posterior and lateral columns of the spinal cord, mainly at thoraciclumbar level. Neuropathy of central nervous system is unknown since no patient has died of EN.

Adult↗
PubMed1998

Autonomic cardiovascular neuropathy in Sjögren's syndrome. A controlled study.

OBJECTIVE: To test patients with primary Sjögren's syndrome (SS) for evidence of autonomic neuropathy. METHODS: Thirty-two patients with primary SS and 22 age and sex matched healthy individuals were asked specific questions about symptoms suggestive of autonomic neuropathy, and were subjected to a battery of 5 cardiovascular tests: response of blood pressure to sustained hand grip, Valsalva maneuver, heart rate response to deep breathing, and heart rate and blood pressure response to standing up. The chi-squared test with Yates' correction and 95% confidence intervals were used for statistical analysis of the results. RESULTS: Sixteen patients (50%) had symptoms of autonomic neuropathy when specifically asked versus none of the controls (p < 0.0005). The frequency of abnormal responses to the tests was 68.8% in patients and 12.7% in controls (p < 0.0001). Severe autonomic cardiovascular neuropathy was found in 87.5% of the patients but in none of the healthy individuals (p < 0.0001). CONCLUSION: Our results suggest that autonomic neuropathy is a feature of a significant portion of the SS population, and such patients should have appropriate evaluation. Similarly, patients with unexplained autonomic neuropathy should be investigated for evidence of SS.

Adult↗
PubMed1998

[Peripheral neuropathies and chronic hepatitis C: a frequent association?].

OBJECTIVE: The aim of this prospective study was to evaluate the prevalence of the peripheral neuropathies associated with chronic hepatitis C and their clinical, electrophysiological and histological characteristics. PATIENTS AND METHODS: Thirty six patients admitted from December 1994 to January 1996 for chronic hepatitis C were prospectively investigated. Laboratory data included liver blood tests, serum cryoprecipitate immunoelectrophoresis, assays for anti-nuclear antibody, rheumatoid factor, circulating immune complexes, anti-SSA and anti-SSB antibodies. For each patient, a clinical neurological evaluation as well as an electrophysiological evaluation were performed by the same operator. In presence of peripheral neuropathy, a neuromuscular biopsy was performed. RESULTS: In seven patients (19%), a peripheral neuropathy was diagnosed related to hepatitis C virus in 3 patients. In these 3 patients presenting with leg paresthesia, an axonal sensitive neuropathy was evidenced by electromyography. A neuromuscular biopsy performed in two of these patients showed a severe diminution of the myelinated fibers associated with vasculitis lesions in one patient. A skin biopsy was performed in the third patient with leg purpura revealing a leukocytoclasic vasculitis. A positive cryoglobulinemia was found in two of these patients. CONCLUSION: In chronic hepatitis C, the prevalence of peripheral neuropathy is 8% and usually associated with cryoglobulinemia. It is an axonal neuropathy with diminution of the myelinated fibers and vasculitis lesions in the absence of cryoglobulinemia.

Adult↗
PubMed2006

Incidence of common compressive neuropathies in primary care.

Apart from carpal tunnel syndrome, there are no population based studies of the epidemiology of compressive neuropathies. To provide this information, new presentations of compressive neuropathies among patients registered with 253 general practices in the UK General Practice Research Database with 1.83 million patient years at risk in 2000 were analysed. The study revealed that in 2000 the annual age standardised rates per 100 000 of new presentations in primary care were: carpal tunnel syndrome, men 87.8/women 192.8; Morton's metatarsalgia, men 50.2/women 87.5; ulnar neuropathy, men 25.2/women 18.9; meralgia paraesthetica, men 10.7/women 13.2; and radial neuropathy, men 2.97/women 1.42. New presentations were most frequent at ages 55-64 years except for carpal tunnel syndrome, which was most frequent in women aged 45-54 years, and radial nerve palsy, which was most frequent in men aged 75-84 years. In 2000, operative treatment was undertaken for 31% of new presentations of carpal tunnel syndrome, 3% of Morton's metatarsalgia, and 30% of ulnar neuropathy.

Adult↗
PubMed2003

[Hereditary sensory and autonomic neuropathy type 2: two cases report].

Two cases of hereditary sensory and autonomic neuropathy type 2 are reported. This type of neuropathy is included in a group that consists of five different entities. The systematization of that neuropathies depends on multiple criteria such as age of beginning, genetic aspects, clinical manifestations, eletroneuromyographic and pathologic features. In this report we describe the cases in a family, two brothers, 27 and 35 years old that were observed in our department with pain insensibility and consequent sensitive-trophic disturbs and deformity of members. The diagnoses was defined as hereditary sensory and autonomic neuropathy type 2 and an inherited pattern recessive autossomic transmission was considered. The age of beginning, the hereditary aspects, the clinical manifestations and the eletroneuromyographic features are analysed. The differential diagnoses with other sensory hereditary and acquired neuropathies is emphasized.

Adult↗