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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurological diseases are frequently associated with axonal degeneration, which leads to dysfunction though separation of neurons from their targets. The mechanisms of axonal degeneration are largely unknown and in many cases are independent of those occurring within cell bodies in neurodegenerative disorders. The Wld(s) mouse mutant demonstrates the unique phenotype of resistance to axonal degeneration after axotomy (slow Wallerian degeneration), making it a powerful tool for studying mechanisms of axonal degeneration. We asked whether the Wld(s) mutation also provides resistance to axonal degeneration in a slowly progressing neuropathy. Using cultured dorsal root ganglion neurons we compared the course of axonal degeneration in response to exposure to the neurotoxin vincristine and found that Wld(s) neurites were relatively resistant to vincristine neuropathy. These findings suggest common pathophysiologic mechanisms between axotomy-induced Wallerian degeneration and toxic neuropathy. The implications are wide-ranging and are relevant to the pathophysiology of axonal degeneration seen in a wide spectrum of neurological diseases ranging from stroke and head trauma to spinal cord injury and peripheral neuropathy.
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PMID:The gene for slow Wallerian degeneration (Wld(s)) is also protective against vincristine neuropathy. 1116 49

In Africa, a rise in complications of diabetes mellitus has gone in hand with the growing disease prevalence, clearly demonstrating the importance of assessing complications. Diabetes mellitus constitutes a major financial burden in developing countries in Africa with relatively limited resources. Ketoacidosis is observed in 24% of juvenile diabetes and is the inaugural sign in 76% of all cases, progressing to coma in 34%. Even in type 2 diabetes, acidoketosis occurs in 34% of the cases. Infection is particularly frequent and is often fatal in tropical Africa because of the involvement of Staphyococcus and Gram-negative microorganisms. Hyperleukocytosis and anemia are correlated with ineffective antibiotic therapy. Pulmonary tuberculosis is the ninth most frequent complication of diabetes. Overall mortality is 14.9 per 1000 person-years of diabetes. Mean age at death is 51.6 years for women and 57.6 years for men after a mean 12.5 year disease duration. Thirty percent of all deaths result from acute metabolic complications, infections and stroke. More than half of the patients with insulin-dependent-diabetes have retinopathy. Differences observed in patients with different ethnic origins is linked basically to unfavorable social and economic conditions that worsen the risk of poor blood glucose control. Retinopathy accounts for 32% of all ocular complications, similar to other African data and more generally in ophthalmology centers. The rate of neuropathy is high, reaching 70% in patients with microangiopathy. Impotence concerns 48.7% of the diabetic population with a mean age of 41.4+/-15.5 years. Coronary artery disease had a recognized influence on hemoglobin diseases, particularly when the coronarography is normal. Lower limb arteriopathy is observed in 18% of the diabetic patients.
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PMID:[Main complications of diabetes mellitus in Africa]. 1117 5

Mitochondria are the principal site of generation of energy in form of adenosine triphosphate (ATP). They contain the enzymes of the Krebs and fatty acid cycles and the respiratory pathway. Ocular tissues with high energy consumption and dependence on oxidative energy production like the optic nerve, the retina, and the pigment epithelium are often involved in mitochondrial diseases. This article reviews the genetic mitochondrial diseases involving the visual system. Their most important ocular findings include: acute or slowly progressive bilateral visual loss and visual field loss due to an optic neuropathy or retinal degeneration, bilateral progressive decreased ocular motility, and bilateral upper lid ptosis. The following diseases are discussed: Leber's Hereditary Optic Neuropathy (LHON); Kearns-Sayre Syndrom (KSS); Chronic Progressive External Ophthalmoplegia (CPEO); Autosomal Recessive Cardiomyopathy, Ophthalmoplegia (ARCO); Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke-Like Episodes (MELAS); Neuropathy, Ataxia, Retinitis Pigmentosa (NARP); Mitochondrial Neuropathy, Gastro-Intestinal Encephalomyopathy (MNGIE); Myoclonus Epilepsy, Ragged-Red-Fibers (MERRF); Wilson's disease; Friedreich's ataxia. Diagnosis of mitochondrial encephalomyopathies is established by screening for mutations in blood or muscle biopsy samples. No specific therapies which influence the course of mitochondrial encephalomyopathies are known. Drugs interacting with the mitochondria function, alcohol consumption and smoking should be avoided.
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PMID:[Eye diseases in mitochondrial encephalomyopathies]. 1121 87

We have examined electroencephalography (EEG) and Mini-Mental State Examination (MMSE) in 38 patients with verified diagnosis of systemic lupus erythematosus (SLE). In the clinical neurological finding there were epileptic attacks in 9 patients, 10 patients suffered from stroke, 15 patients from lupus headache, 4 patients from psychosis, in 15 patients cranial neuropathy was present, in one person extrapyramidal syndrome. EEG findings were in 12 patients normal (32%), in 26 patients abnormal (66%). In 3 cases there were focal abnormalities (8%), in 19 cases episodic ones (48%), four times abnormalities were diffuse (10%). Diffuse abnormalities correlated in EEG findings with case history of GM attacks.
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PMID:[EEG findings in patients with systemic lupus erythematosus]. 1122 81

A number of diseases of the nervous system, especially upper neuron lesions, produce ankle and foot deformities. Such deformities can be the single most important reason why some patients become nonambulatory. This article reviews the impact of upper motor neuron lesions such as traumatic brain injury, stroke, multiple sclerosis, neurodegenerative disorders, and low motor neuron lesions such as peripheral nerve injury, neuropathy, entrapment syndromes, and muscle diseases. This article also reviews diagnostic tests including EMG and nonsurgical management.
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PMID:Nerve and muscle disorders and their sequelae. 1123 27

A major government-sponsored study of nerve growth factor for treating HIV-related neuropathy has recently been revived after it was canceled earlier this year by Genentech, Inc. of South San Francisco, which holds a patent for the use of the drug. Human nerve growth factor has been shown to be the most promising therapy for treating HIV-related neuropathy, the most common neurological complication in AIDS. The AIDS Clinical Trials Group (ACTG) of the National Institute of Allergy and Infectious Disease and the National Institute of Neurological Disorders and Stroke have, for three years, been developing a study of 180 randomly assigned volunteers to receive low-dose nerve growth factor, high-dose nerve growth factor, or placebo. However, in January 1995, Genentech informed the government that it would not provide the drug--although almost all of the financial cost of the study was to be paid for by the ACTG. After major protests by experts and community organizations, Genentech reinstated its earlier agreement to provide the drug for the ACTG study. The trial, known as ACTG 291, is expected to go forward.
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PMID:Nerve growth factor: major trial canceled, revived after protest. 1136 4

We report three members of a family, who exhibited a phenotype similar to 'myoclonus epilepsy with ragged-red fibers' but had a genotype usually associated with 'mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes'. The patients, a 48-year-old female, and her two sons, aged 21 and 19 respectively, presented with photo-reactive syncopal episodes, disturbances of gait and writing, dysarthria and finger tremor since the 3rd and 2nd decade of life, respectively, that were accompanied also by numbness and weakness of the extremities. Subsequently, cerebellar ataxia and myoclonus were also noted. Electromyography revealed both myogenic and neurogenic muscular changes, and nerve conduction studies demonstrated a sensory-motor neuropathy. Biopsy showed ragged-red fibers with strongly stained SDH-positive vessels in skeletal muscles, and a marked loss of myelinated fibers of the sural nerves. Mitochondrial (mt) DNA analyses of peripheral blood, muscles and nerves revealed that all members had a heteroplasmic np3271 (T-C) point mutation in the mitochondrial tRNA-Leu gene (UUR). This family is unique, in that all patients presented with a myoclonus epilepsy with ragged-red fibers-like phenotype and had a distinctive peripheral neuropathy, while the detected mtDNA 327l (T-C) mutation has been reported to date only in rare cases of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes
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PMID:A mitochondrial encephalo-myo-neuropathy with a nucleotide position 3271 (T-C) point mutation in the mitochondrial DNA. 1140 19

We present a case of a 69-year-old woman who developed brachial plexopathy and long thoracic nerve palsy secondary to compression from a hematoma while receiving heparin therapy for the treatment of a stroke. The patient was treated conservatively with discontinuation of heparin and had complete resolution of her compressive neuropathy. This is the first report of a patient with long thoracic nerve palsy with a brachial plexopathy complicating anticoagulation. We review the literature on hematoma-induced compressive neuropathies and treatment options. Our review concludes by emphasizing the importance of clinical judgment in determining the best therapeutic modality.
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PMID:Compressive neuropathy of the brachial plexus and long thoracic nerve: a rare complication of heparin anticoagulation. 1145 57

Diabetic nephropathy is a leading cause of end-stage renal disease, and its prevalence and incidence vary greatly from country to country, being highest in the United States and Japan. In the United States, diabetic nephropathy accounts for approximately 40% of patients beginning renal replacement therapy. Type 2 diabetes is the largest and fastest-growing single disease that requires dialytic therapy. Most patients succumb to cardiovascular causes, including coronary artery disease and myocardial infarction, sudden death, cardiac failure, and stroke. The survival from cardiovascular complications is relatively better in East Asian countries and to a lesser extent in Mediterranean countries compared with countries that traditionally have higher cardiovascular death rates. Peripheral vascular disease and sepsis contribute to increased morbidity and mortality. Amputation of limbs secondary to peripheral vascular disease in particular has adverse effects on rehabilitation. Asymptomatic hypoglycemia may develop in hemodialysis patients. Such hypoglycemia is not associated with a hormonal balance but is postulated to be due to blunted hormonal response to hypoglycemia. Diabetic muscle infarction is another rare complication attributable to diabetic microangiopathy; magnetic resonance imaging may help in the diagnosis. Risk factors for increased mortality include advanced age, poor glycemic control before starting dialysis, smoking, left ventricular hypertrophy, hypoalbuminemia, and neuropathy, in particular, autonomic dysfunction. In addition to adequate dialysis, it is advisable to achieve tight blood pressure control (at least <140/90 mm Hg and preferably much lower), better blood glucose control (hemoglobin A(1c), <7%), correction of nutritional status, and appropriate foot care.
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PMID:Hemodialysis in diabetic patients. 1157 54

The aim of this study was to provide an overview of diabetes management and complication status in Taiwan. A cohort of 2446 patients (from 25 diabetic centers) with more than 12 months of diabetes management participated and data were collected by interviews and reviewing the medical records. Overall, 97% were diagnosed as type 2 diabetes, with a mean age (+/-S.D.) of 61.6+/-11.3 years, duration of diabetes of 10.3+/-7.3 years and age at onset of diabetes of 51.5+/-11.8 years. Mean BMI was 25.1+/-3.6 kg/m(2) and about 50% had BMI>25 kg/m(2). Majority (75%) were treated with oral hypoglycemic agents (OHAs), 14% with insulin and 10% with combination of insulin and OHA. Mean HbA(1c) was 8.1+/-1.6% and 59% had HbA(1c) >7.4% (1% above the upper limit of normal range, 4.7-6.4%). Mean FBG was 9.0+/-3.3 mmol/l and 59% had FBG>7.8 mmol/l. Of all the patients who had screening for complications, cataract (38%), neuropathy (30%), proteinuria (17%) and stroke (6%) were the most frequently reported eye, feet, kidney and late complications. We conclude that the majority of patients involved in this study had unsatisfactory glycaemic control which may lead to diabetes complications.
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PMID:The current state of diabetes management in Taiwan. 1158 Sep 70


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